Nutrient chapter

Mangiferin

Mangiferin is a C-glucosyl xanthone (CAS 4773-96-0), distinct from mango fruit, bark or leaf extracts, its monosodium formulation, and the aglycone norathyriol. Preparation, microbial conversion, concentration and tissue determine the scope of each recorded finding. No essential dietary requirement or specific mangiferin-deficiency syndrome is established.

104 recorded mechanisms · 4 availability situations · 5 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

An inducible activity in Bacteroides sp. MANG cleaved mangiferin to norathyriol.
Bacteroides sp. MANG inducible C-glucosyl-cleaving activity, molecular identity unresolved → Norathyriol source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"}
experimental_model
Isolated anaerobic human-fecal bacterium and cell-free extracts
exposure
Mangiferin culture exposure, with transcription/translation inhibitors
limitations
One isolate; activity identity unresolved; not a prediction of every human microbiome.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Bacteroides sp. MANG
plain_language
A bacterial system removes the attached sugar.
primary_references
[mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
tissue_or_cell_type
Bacterial culture
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 106–117
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated anaerobic human-fecal bacterium and cell-free extracts · source_derived_draft · unverified_draft
### mangiferin-bacterial-cleavage An inducible activity in Bacteroides sp. MANG cleaved mangiferin to norathyriol. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A bacterial system removes the attached sugar. organism: Bacteroides sp. MANG tissue_or_cell_type: Bacterial culture experimental_model: Isolated anaerobic human-fecal bacterium and cell-free extracts limitations: One isolate; activity identity unresolved; not a prediction of every human microbiome. exposure: Mangiferin culture exposure, with transcription/translation inhibitors evidence_span: {"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"} [mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
Complete structured claim and evidence
After 0.9 g orally, plasma mangiferin peaked at 38.64 +/- 6.75 ng/mL at about one hour; apparent half-life was 7.85 +/- 1.72 hours.
Mangiferin → Human circulating mangiferin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26434292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d", "start_char": 0, "end_char": 1251, "text_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d"}
experimental_model
Single-dose human pharmacokinetic study
exposure
Single oral 0.1, 0.3 or 0.9 g mangiferin
limitations
Small pharmacokinetic study; no intravenous comparator or demonstration of cellular target engagement.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
21 healthy Chinese men
plain_language
Oral intake produced measurable but low circulating parent compound.
primary_references
[mangiferin-p26434292] Pharmacokinetic study of mangiferin in human plasma after oral administration. (2012). https://pubmed.ncbi.nlm.nih.gov/26434292/ DOI: 10.1016/j.foodchem.2011.10.079
tissue_or_cell_type
Plasma
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 236–247
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose human pharmacokinetic study · source_derived_draft · unverified_draft
### mangiferin-human-pk After 0.9 g orally, plasma mangiferin peaked at 38.64 +/- 6.75 ng/mL at about one hour; apparent half-life was 7.85 +/- 1.72 hours. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oral intake produced measurable but low circulating parent compound. organism: 21 healthy Chinese men tissue_or_cell_type: Plasma experimental_model: Single-dose human pharmacokinetic study limitations: Small pharmacokinetic study; no intravenous comparator or demonstration of cellular target engagement. exposure: Single oral 0.1, 0.3 or 0.9 g mangiferin evidence_span: {"source_cache": "artifacts/mangiferin-research/26434292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d", "start_char": 0, "end_char": 1251, "text_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d"} [mangiferin-p26434292] Pharmacokinetic study of mangiferin in human plasma after oral administration. (2012). https://pubmed.ncbi.nlm.nih.gov/26434292/ DOI: 10.1016/j.foodchem.2011.10.079
Complete structured claim and evidence
Mangiferin prevented ascorbate-driven ferric iron reduction in vitro.
Mangiferin → Ascorbate-driven reduction of ferric iron in vitro source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"}
experimental_model
Isolated mitochondrial and iron-redox assays
exposure
10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment
limitations
In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
Iron binding changed a reaction involving vitamin C.
primary_references
[mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
tissue_or_cell_type
Liver mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 692–703
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated mitochondrial and iron-redox assays · source_derived_draft · unverified_draft
### mangiferin-iron-vitamin-c Mangiferin prevented ascorbate-driven ferric iron reduction in vitro. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron binding changed a reaction involving vitamin C. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Liver mitochondria experimental_model: Isolated mitochondrial and iron-redox assays limitations: In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload. exposure: 10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"} [mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
Complete structured claim and evidence
Mangiferin exposure increased susceptibility to calcium-induced mitochondrial permeability transition.
Mangiferin → Rat liver mitochondrial permeability transition source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/15979560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f", "start_char": 0, "end_char": 2234, "text_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f"}
experimental_model
Rat pretreatment and isolated mitochondrial calcium challenge
exposure
40 mg/kg mangiferin pretreatment; isolated mitochondria exposed to calcium
limitations
Mitochondrial challenge does not establish harm from usual oral intake; proposed quinone-thiol adduct mechanism was not fully proven.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
Lower oxidative readouts do not necessarily mean preserved membrane function.
primary_references
[mangiferin-p15979560] Mangiferin, a natural occurring glucosyl xanthone, increases susceptibility of rat liver mitochondria to calcium-induced permeability transition. (2005). https://pubmed.ncbi.nlm.nih.gov/15979560/ DOI: 10.1016/j.abb.2005.05.015
tissue_or_cell_type
Liver mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 705–716
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pretreatment and isolated mitochondrial calcium challenge · source_derived_draft · unverified_draft
### mangiferin-calcium-mpt Mangiferin exposure increased susceptibility to calcium-induced mitochondrial permeability transition. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lower oxidative readouts do not necessarily mean preserved membrane function. organism: Rattus norvegicus tissue_or_cell_type: Liver mitochondria experimental_model: Rat pretreatment and isolated mitochondrial calcium challenge limitations: Mitochondrial challenge does not establish harm from usual oral intake; proposed quinone-thiol adduct mechanism was not fully proven. exposure: 40 mg/kg mangiferin pretreatment; isolated mitochondria exposed to calcium evidence_span: {"source_cache": "artifacts/mangiferin-research/15979560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f", "start_char": 0, "end_char": 2234, "text_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f"} [mangiferin-p15979560] Mangiferin, a natural occurring glucosyl xanthone, increases susceptibility of rat liver mitochondria to calcium-induced permeability transition. (2005). https://pubmed.ncbi.nlm.nih.gov/15979560/ DOI: 10.1016/j.abb.2005.05.015
Complete structured claim and evidence
The ferric complex did not elicit permeability transition and protected against its induction in the assay.
Mangiferin-ferric iron complex, assay-defined → Rat liver mitochondrial permeability transition source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"}
experimental_model
Iron-coordination spectroscopy and mitochondrial challenge
exposure
Assay-defined ferric iron-mangiferin complex
limitations
Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
Changing chemical form changed the membrane response.
primary_references
[mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
tissue_or_cell_type
Isolated mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 744–755
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Iron-coordination spectroscopy and mitochondrial challenge · source_derived_draft · unverified_draft
### mangiferin-complex-mpt The ferric complex did not elicit permeability transition and protected against its induction in the assay. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing chemical form changed the membrane response. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Isolated mitochondria experimental_model: Iron-coordination spectroscopy and mitochondrial challenge limitations: Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation. exposure: Assay-defined ferric iron-mangiferin complex evidence_span: {"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"} [mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
Complete structured claim and evidence
PDH activity increased in assays using mitochondrial protein from mangiferin-treated C2C12 cells.
Mangiferin → Mouse pyruvate dehydrogenase complex source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
Dietary mangiferin in mice; pharmacological cell exposures
limitations
Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
An enzyme complex linking glycolysis to mitochondrial metabolism became more active.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-pdh-activity PDH activity increased in assays using mitochondrial protein from mangiferin-treated C2C12 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme complex linking glycolysis to mitochondrial metabolism became more active. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency. exposure: Dietary mangiferin in mice; pharmacological cell exposures evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation.
Experimental human STK11 / LKB1 siRNA knockdown → Human AMP-activated protein kinase complexes source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
Removing an upstream component interrupted the response.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 497–508
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-lkb1-ampk LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
Mangiferin opposed H2O2-associated loss of manganese superoxide dismutase expression and activity.
Mangiferin → Human mitochondrial manganese superoxide dismutase / SOD2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
experimental_model
Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
exposure
Mangiferin before H2O2 exposure
limitations
Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
An enzyme that depends on manganese was part of the measured response.
primary_references
[mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
tissue_or_cell_type
ARPE-19 retinal pigment epithelial cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 614–625
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft
### mangiferin-rpe-sod2 Mangiferin opposed H2O2-associated loss of manganese superoxide dismutase expression and activity. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme that depends on manganese was part of the measured response. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
Complete structured claim and evidence
Norathyriol competitively inhibited UGT1A9; IC50 12.3 and Ki 2.8 micromolar.
Norathyriol → Human UDP-glucuronosyltransferase 1A9 / UGT1A9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"}
experimental_model
Recombinant UGT inhibition kinetics
exposure
Micromolar norathyriol; initial comparison at 100 micromolar
limitations
Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Recombinant enzyme assay
plain_language
The aglycone has its own conjugation-enzyme interaction profile.
primary_references
[mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
tissue_or_cell_type
4-methylumbelliferone glucuronidation
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 900–911
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant UGT inhibition kinetics · source_derived_draft · unverified_draft
### mangiferin-norathyriol-ugt1a9 Norathyriol competitively inhibited UGT1A9; IC50 12.3 and Ki 2.8 micromolar. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The aglycone has its own conjugation-enzyme interaction profile. organism: Recombinant enzyme assay tissue_or_cell_type: 4-methylumbelliferone glucuronidation experimental_model: Recombinant UGT inhibition kinetics limitations: Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo. exposure: Micromolar norathyriol; initial comparison at 100 micromolar evidence_span: {"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"} [mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
Complete structured claim and evidence
Serum triglycerides were lower with mangiferin than placebo.
Mangiferin → Human serum triglyceride concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
A blood lipid endpoint improved in this trial.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1147–1158
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-tg Serum triglycerides were lower with mangiferin than placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A blood lipid endpoint improved in this trial. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Serum L-carnitine increased compared with placebo.
Mangiferin → Human serum L-carnitine concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
A metabolite used in fatty-acid handling was higher in blood.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1199–1210
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-carnitine Serum L-carnitine increased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A metabolite used in fatty-acid handling was higher in blood. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Serum glucose did not differ significantly between groups.
Mangiferin → Serum glucose concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
The trial did not demonstrate improvement in every glucose endpoint.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1251–1262
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-glucose-null Serum glucose did not differ significantly between groups. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not demonstrate improvement in every glucose endpoint. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
The rifampicin treatment abolished the induced C-glucosyl-cleaving activity.
Rifampicin → Bacteroides sp. MANG inducible C-glucosyl-cleaving activity, molecular identity unresolved source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"}
experimental_model
Isolated anaerobic human-fecal bacterium and cell-free extracts
exposure
Mangiferin culture exposure, with transcription/translation inhibitors
limitations
One isolate; activity identity unresolved; not a prediction of every human microbiome.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Bacteroides sp. MANG
plain_language
Conversion requires functioning bacterial gene-expression machinery.
primary_references
[mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
tissue_or_cell_type
Bacterial culture
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 119–130
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated anaerobic human-fecal bacterium and cell-free extracts · source_derived_draft · unverified_draft
### mangiferin-rifampicin-cleavage The rifampicin treatment abolished the induced C-glucosyl-cleaving activity. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Conversion requires functioning bacterial gene-expression machinery. organism: Bacteroides sp. MANG tissue_or_cell_type: Bacterial culture experimental_model: Isolated anaerobic human-fecal bacterium and cell-free extracts limitations: One isolate; activity identity unresolved; not a prediction of every human microbiome. exposure: Mangiferin culture exposure, with transcription/translation inhibitors evidence_span: {"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"} [mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
Complete structured claim and evidence
The chloramphenicol treatment abolished the induced C-glucosyl-cleaving activity.
Chloramphenicol → Bacteroides sp. MANG inducible C-glucosyl-cleaving activity, molecular identity unresolved source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"}
experimental_model
Isolated anaerobic human-fecal bacterium and cell-free extracts
exposure
Mangiferin culture exposure, with transcription/translation inhibitors
limitations
One isolate; activity identity unresolved; not a prediction of every human microbiome.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Bacteroides sp. MANG
plain_language
Conversion requires functioning bacterial gene-expression machinery.
primary_references
[mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
tissue_or_cell_type
Bacterial culture
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 132–143
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated anaerobic human-fecal bacterium and cell-free extracts · source_derived_draft · unverified_draft
### mangiferin-chloramphenicol-cleavage The chloramphenicol treatment abolished the induced C-glucosyl-cleaving activity. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Conversion requires functioning bacterial gene-expression machinery. organism: Bacteroides sp. MANG tissue_or_cell_type: Bacterial culture experimental_model: Isolated anaerobic human-fecal bacterium and cell-free extracts limitations: One isolate; activity identity unresolved; not a prediction of every human microbiome. exposure: Mangiferin culture exposure, with transcription/translation inhibitors evidence_span: {"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"} [mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
Complete structured claim and evidence
Fecal cultures converted mangiferin to norathyriol with donor-dependent variation.
Mangiferin → Norathyriol source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"}
experimental_model
Ex vivo human fecal fermentation and metagenomic profiling
exposure
Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation
limitations
Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Human-derived microbial communities
plain_language
Different microbial communities process the same compound differently.
primary_references
[mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
tissue_or_cell_type
Fecal cultures
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 145–156
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ex vivo human fecal fermentation and metagenomic profiling · source_derived_draft · unverified_draft
### mangiferin-microbial-conversion Fecal cultures converted mangiferin to norathyriol with donor-dependent variation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different microbial communities process the same compound differently. organism: Human-derived microbial communities tissue_or_cell_type: Fecal cultures experimental_model: Ex vivo human fecal fermentation and metagenomic profiling limitations: Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof. exposure: Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation evidence_span: {"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"} [mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
Complete structured claim and evidence
Norathyriol reduced overall bacterial cell counts in the tested cultures.
Norathyriol → Bacterial cell abundance in human fecal cultures source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"}
experimental_model
Ex vivo human fecal fermentation and metagenomic profiling
exposure
Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation
limitations
Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Human-derived microbial communities
plain_language
Its metabolite changed bacterial growth.
primary_references
[mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
tissue_or_cell_type
Fecal cultures
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 158–169
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ex vivo human fecal fermentation and metagenomic profiling · source_derived_draft · unverified_draft
### mangiferin-microbial-count Norathyriol reduced overall bacterial cell counts in the tested cultures. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Its metabolite changed bacterial growth. organism: Human-derived microbial communities tissue_or_cell_type: Fecal cultures experimental_model: Ex vivo human fecal fermentation and metagenomic profiling limitations: Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof. exposure: Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation evidence_span: {"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"} [mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
Complete structured claim and evidence
Norathyriol suppressed Faecalibacterium prausnitzii in the culture comparison.
Norathyriol → Faecalibacterium prausnitzii abundance in fecal cultures source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"}
experimental_model
Ex vivo human fecal fermentation and metagenomic profiling
exposure
Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation
limitations
Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Human-derived microbial communities
plain_language
A short-chain-fatty-acid producer was among the affected microbes.
primary_references
[mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
tissue_or_cell_type
Fecal cultures
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 171–182
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ex vivo human fecal fermentation and metagenomic profiling · source_derived_draft · unverified_draft
### mangiferin-faecalibacterium Norathyriol suppressed Faecalibacterium prausnitzii in the culture comparison. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A short-chain-fatty-acid producer was among the affected microbes. organism: Human-derived microbial communities tissue_or_cell_type: Fecal cultures experimental_model: Ex vivo human fecal fermentation and metagenomic profiling limitations: Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof. exposure: Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation evidence_span: {"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"} [mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
Complete structured claim and evidence
Norathyriol suppressed the urate-consuming species Enterocloster bolteae in culture.
Norathyriol → Enterocloster bolteae abundance in fecal cultures source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"}
experimental_model
Ex vivo human fecal fermentation and metagenomic profiling
exposure
Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation
limitations
Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Human-derived microbial communities
plain_language
The affected community includes microbes that consume urate.
primary_references
[mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
tissue_or_cell_type
Fecal cultures
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 184–195
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ex vivo human fecal fermentation and metagenomic profiling · source_derived_draft · unverified_draft
### mangiferin-enterocloster Norathyriol suppressed the urate-consuming species Enterocloster bolteae in culture. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The affected community includes microbes that consume urate. organism: Human-derived microbial communities tissue_or_cell_type: Fecal cultures experimental_model: Ex vivo human fecal fermentation and metagenomic profiling limitations: Community findings do not establish health benefit or harm in people; candidate converter taxa were associations, not isolated causal proof. exposure: Mangiferin or norathyriol 500 micromolar in culture; not participant supplementation evidence_span: {"source_cache": "artifacts/mangiferin-research/40401774.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380", "start_char": 0, "end_char": 1390, "text_sha256": "56539abd79e79a7968a5ec040d9fff33a864b228236cfecba1c7e0ccd3eae380"} [mangiferin-p40401774] Gut microbiota-mediated conversion of mangiferin to norathyriol alters short chain fatty acid and urate metabolism. (2025). https://pubmed.ncbi.nlm.nih.gov/40401774/ DOI: 10.1080/19490976.2025.2508422
Complete structured claim and evidence
Norathyriol absolute bioavailability was 30.4% in the rat experiment.
Norathyriol → Rat circulating norathyriol exposure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"}
experimental_model
Rat pharmacokinetics and hepatocyte metabolite profiling
exposure
Administered norathyriol; study-specific routes
limitations
Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The aglycone has its own absorption profile.
primary_references
[mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
tissue_or_cell_type
Blood and hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 197–208
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pharmacokinetics and hepatocyte metabolite profiling · source_derived_draft · unverified_draft
### mangiferin-norathyriol-pk Norathyriol absolute bioavailability was 30.4% in the rat experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The aglycone has its own absorption profile. organism: Rattus norvegicus tissue_or_cell_type: Blood and hepatocytes experimental_model: Rat pharmacokinetics and hepatocyte metabolite profiling limitations: Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin. exposure: Administered norathyriol; study-specific routes evidence_span: {"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"} [mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
Complete structured claim and evidence
Norathyriol glucuronides were prominent circulating conjugates after administration in rats.
Norathyriol → Norathyriol glucuronide conjugates, positions unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"}
experimental_model
Rat pharmacokinetics and hepatocyte metabolite profiling
exposure
Administered norathyriol; study-specific routes
limitations
Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
Chemical conjugation changes what circulates; parent compound and conjugates remain separate.
primary_references
[mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
tissue_or_cell_type
Blood and hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 210–221
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pharmacokinetics and hepatocyte metabolite profiling · source_derived_draft · unverified_draft
### mangiferin-glucuronides Norathyriol glucuronides were prominent circulating conjugates after administration in rats. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chemical conjugation changes what circulates; parent compound and conjugates remain separate. organism: Rattus norvegicus tissue_or_cell_type: Blood and hepatocytes experimental_model: Rat pharmacokinetics and hepatocyte metabolite profiling limitations: Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin. exposure: Administered norathyriol; study-specific routes evidence_span: {"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"} [mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
Complete structured claim and evidence
Norathyriol sulfates were prominent circulating conjugates after administration in rats.
Norathyriol → Norathyriol sulfate conjugates, positions unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"}
experimental_model
Rat pharmacokinetics and hepatocyte metabolite profiling
exposure
Administered norathyriol; study-specific routes
limitations
Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
Chemical conjugation changes what circulates; parent compound and conjugates remain separate.
primary_references
[mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
tissue_or_cell_type
Blood and hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 223–234
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pharmacokinetics and hepatocyte metabolite profiling · source_derived_draft · unverified_draft
### mangiferin-sulfates Norathyriol sulfates were prominent circulating conjugates after administration in rats. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chemical conjugation changes what circulates; parent compound and conjugates remain separate. organism: Rattus norvegicus tissue_or_cell_type: Blood and hepatocytes experimental_model: Rat pharmacokinetics and hepatocyte metabolite profiling limitations: Rat absolute bioavailability does not quantify human exposure or conversion from mangiferin. exposure: Administered norathyriol; study-specific routes evidence_span: {"source_cache": "artifacts/mangiferin-research/30298742.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288", "start_char": 0, "end_char": 1196, "text_sha256": "4caff8b6b7f04d6d1adca704cd53190801d3cf39f282bdb4e93b507a72b51288"} [mangiferin-p30298742] Absorption, Metabolism, and Pharmacokinetics Profiles of Norathyriol, an Aglycone of Mangiferin, in Rats by HPLC-MS/MS. (2018). https://pubmed.ncbi.nlm.nih.gov/30298742/ DOI: 10.1021/acs.jafc.8b03763
Complete structured claim and evidence
Human mangiferin pharmacokinetics were nonlinear across the tested doses.
Mangiferin → Human circulating mangiferin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26434292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d", "start_char": 0, "end_char": 1251, "text_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d"}
experimental_model
Single-dose human pharmacokinetic study
exposure
Single oral 0.1, 0.3 or 0.9 g mangiferin
limitations
Small pharmacokinetic study; no intravenous comparator or demonstration of cellular target engagement.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
21 healthy Chinese men
plain_language
Increasing the dose does not imply a proportional exposure increase.
primary_references
[mangiferin-p26434292] Pharmacokinetic study of mangiferin in human plasma after oral administration. (2012). https://pubmed.ncbi.nlm.nih.gov/26434292/ DOI: 10.1016/j.foodchem.2011.10.079
tissue_or_cell_type
Plasma
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 249–260
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose human pharmacokinetic study · source_derived_draft · unverified_draft
### mangiferin-nonlinear-pk Human mangiferin pharmacokinetics were nonlinear across the tested doses. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing the dose does not imply a proportional exposure increase. organism: 21 healthy Chinese men tissue_or_cell_type: Plasma experimental_model: Single-dose human pharmacokinetic study limitations: Small pharmacokinetic study; no intravenous comparator or demonstration of cellular target engagement. exposure: Single oral 0.1, 0.3 or 0.9 g mangiferin evidence_span: {"source_cache": "artifacts/mangiferin-research/26434292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d", "start_char": 0, "end_char": 1251, "text_sha256": "aa87147889d9de521835562b716d5afe1c1458cd33ff3b7ff7ac67494fcfcd7d"} [mangiferin-p26434292] Pharmacokinetic study of mangiferin in human plasma after oral administration. (2012). https://pubmed.ncbi.nlm.nih.gov/26434292/ DOI: 10.1016/j.foodchem.2011.10.079
Complete structured claim and evidence
MLES produced 2.44-fold higher AUC over 24 hours than MLE60 in the crossover comparison.
Mango leaf extract MLES, monosodium mangiferin preparation → Human circulating mangiferin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/39942566.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f3b135e29a0a2b6268f49880822ee862a25c62b401ef8046a5feb1667b06330", "start_char": 0, "end_char": 1283, "text_sha256": "7f3b135e29a0a2b6268f49880822ee862a25c62b401ef8046a5feb1667b06330"}
experimental_model
Human crossover pharmacokinetic comparison
exposure
Two standardized 60% mango-leaf extracts; seven-day washout
limitations
Relative exposure comparison of formulations, not absolute bioavailability, pure-compound equivalence or demonstrated clinical benefit.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
12 adults, six women
plain_language
The soluble salt preparation changed circulating exposure.
primary_references
[mangiferin-p39942566] Human Pharmacokinetic Profiling and Comparative Analysis of Mangiferin and Its Monosodium Derivative from Mangifera indica Extracts Using UHPLC-MS/MS with 1H NMR and MALDI-TOF Confirmation. (2025). https://pubmed.ncbi.nlm.nih.gov/39942566/ DOI: 10.3390/molecules30030461
tissue_or_cell_type
Plasma
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 262–273
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human crossover pharmacokinetic comparison · source_derived_draft · unverified_draft
### mangiferin-salt-exposure MLES produced 2.44-fold higher AUC over 24 hours than MLE60 in the crossover comparison. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The soluble salt preparation changed circulating exposure. organism: 12 adults, six women tissue_or_cell_type: Plasma experimental_model: Human crossover pharmacokinetic comparison limitations: Relative exposure comparison of formulations, not absolute bioavailability, pure-compound equivalence or demonstrated clinical benefit. exposure: Two standardized 60% mango-leaf extracts; seven-day washout evidence_span: {"source_cache": "artifacts/mangiferin-research/39942566.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f3b135e29a0a2b6268f49880822ee862a25c62b401ef8046a5feb1667b06330", "start_char": 0, "end_char": 1283, "text_sha256": "7f3b135e29a0a2b6268f49880822ee862a25c62b401ef8046a5feb1667b06330"} [mangiferin-p39942566] Human Pharmacokinetic Profiling and Comparative Analysis of Mangiferin and Its Monosodium Derivative from Mangifera indica Extracts Using UHPLC-MS/MS with 1H NMR and MALDI-TOF Confirmation. (2025). https://pubmed.ncbi.nlm.nih.gov/39942566/ DOI: 10.3390/molecules30030461
Complete structured claim and evidence
The spray-dried cashew-pectin system encapsulated mangiferin with reported efficiency of 82.02%.
Cashew apple pectin, preparation specified by study → Mangiferin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/33422511.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94f03b6027f5e127135766a609b273a2ba7347687f229c99c4357f21f91b1aa2", "start_char": 0, "end_char": 922, "text_sha256": "94f03b6027f5e127135766a609b273a2ba7347687f229c99c4357f21f91b1aa2"}
experimental_model
Formulation characterization, release testing and isolated human-neutrophil evaluation
exposure
Spray-dried cashew-apple pectin and mangiferin; release media at specified pH
limitations
No oral human bioavailability result; matrix behavior cannot be generalized to eating pectin with mangiferin.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Material system and human cells
plain_language
Pectin can serve as a delivery material in a deliberately prepared formulation.
primary_references
[mangiferin-p33422511] Cashew apple pectin as a carrier matrix for mangiferin: Physicochemical characterization, in vitro release and biological evaluation in human neutrophils. (2021). https://pubmed.ncbi.nlm.nih.gov/33422511/ DOI: 10.1016/j.ijbiomac.2021.01.001
tissue_or_cell_type
Pectin matrix and neutrophils
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 275–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Formulation characterization, release testing and isolated human-neutrophil evaluation · source_derived_draft · unverified_draft
### mangiferin-pectin-matrix The spray-dried cashew-pectin system encapsulated mangiferin with reported efficiency of 82.02%. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pectin can serve as a delivery material in a deliberately prepared formulation. organism: Material system and human cells tissue_or_cell_type: Pectin matrix and neutrophils experimental_model: Formulation characterization, release testing and isolated human-neutrophil evaluation limitations: No oral human bioavailability result; matrix behavior cannot be generalized to eating pectin with mangiferin. exposure: Spray-dried cashew-apple pectin and mangiferin; release media at specified pH evidence_span: {"source_cache": "artifacts/mangiferin-research/33422511.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94f03b6027f5e127135766a609b273a2ba7347687f229c99c4357f21f91b1aa2", "start_char": 0, "end_char": 922, "text_sha256": "94f03b6027f5e127135766a609b273a2ba7347687f229c99c4357f21f91b1aa2"} [mangiferin-p33422511] Cashew apple pectin as a carrier matrix for mangiferin: Physicochemical characterization, in vitro release and biological evaluation in human neutrophils. (2021). https://pubmed.ncbi.nlm.nih.gov/33422511/ DOI: 10.1016/j.ijbiomac.2021.01.001
Complete structured claim and evidence
Mangiferin increased glucose oxidation in the studied mouse-muscle systems.
Mangiferin → Glucose oxidation in mouse muscle-cell models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
Dietary mangiferin in mice; pharmacological cell exposures
limitations
Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
More glucose-derived fuel entered oxidative metabolism.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-glucose-oxidation Mangiferin increased glucose oxidation in the studied mouse-muscle systems. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glucose-derived fuel entered oxidative metabolism. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency. exposure: Dietary mangiferin in mice; pharmacological cell exposures evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
Mangiferin increased pyruvate oxidation in C2C12 myotubes.
Mangiferin → Pyruvate oxidation in mouse muscle-cell models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
Dietary mangiferin in mice; pharmacological cell exposures
limitations
Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
The downstream product of glycolysis was used more oxidatively.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 301–312
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-pyruvate-oxidation Mangiferin increased pyruvate oxidation in C2C12 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The downstream product of glycolysis was used more oxidatively. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency. exposure: Dietary mangiferin in mice; pharmacological cell exposures evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
Mangiferin reduced anaerobic pyruvate-to-lactate metabolism in the cell experiments.
Mangiferin → Lactate production in mouse muscle-cell models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
Dietary mangiferin in mice; pharmacological cell exposures
limitations
Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
Pyruvate handling shifted away from lactate production.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 314–325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-lactate Mangiferin reduced anaerobic pyruvate-to-lactate metabolism in the cell experiments. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pyruvate handling shifted away from lactate production. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency. exposure: Dietary mangiferin in mice; pharmacological cell exposures evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
Mangiferin did not increase fatty acid oxidation in these muscle-cell experiments.
Mangiferin → Fatty acid oxidation in mouse muscle-cell models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
Dietary mangiferin in mice; pharmacological cell exposures
limitations
Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
The fuel shift was not an increase in every oxidation pathway.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 327–338
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-fat-oxidation-null Mangiferin did not increase fatty acid oxidation in these muscle-cell experiments. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The fuel shift was not an increase in every oxidation pathway. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Preclinical experiments; no proof of direct binding or correction of human vitamin deficiency. exposure: Dietary mangiferin in mice; pharmacological cell exposures evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251", "start_char": 0, "end_char": 1761, "text_sha256": "5f12809489e236c3dd9888aae3746eb22ff9cbea4271c9f60764bed3b5f9d251"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
After 24 hours, mangiferin reduced PDK4 protein abundance in C2C12 cells.
Mangiferin → Mouse pyruvate dehydrogenase kinase 4 / Pdk4 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cbbc4a9b075ae11f5b88a9929a65c77e6b39870068e320a281bd1802384fec8", "start_char": 30977, "end_char": 31862, "text_sha256": "8e9b4448f5213862fa4c8b78f1d49c9f6b4e6faffb97d818dabbd4117d386dba"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
200 or 1000 micromolar mangiferin, 24 hours; Figure 6
limitations
Cell exposure well above the parent plasma concentrations reported in the selected human PK study; reduced expression is not direct kinase-binding evidence.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
Longer exposure reduced a kinase that restrains PDH.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 353–364
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-pdk4 After 24 hours, mangiferin reduced PDK4 protein abundance in C2C12 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Longer exposure reduced a kinase that restrains PDH. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: Cell exposure well above the parent plasma concentrations reported in the selected human PK study; reduced expression is not direct kinase-binding evidence. exposure: 200 or 1000 micromolar mangiferin, 24 hours; Figure 6 evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cbbc4a9b075ae11f5b88a9929a65c77e6b39870068e320a281bd1802384fec8", "start_char": 30977, "end_char": 31862, "text_sha256": "8e9b4448f5213862fa4c8b78f1d49c9f6b4e6faffb97d818dabbd4117d386dba"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
After 15 minutes, PDH phosphorylation decreased without a detected change in PDK4 abundance.
Mangiferin → Mouse muscle pyruvate dehydrogenase phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24848064.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cbbc4a9b075ae11f5b88a9929a65c77e6b39870068e320a281bd1802384fec8", "start_char": 30977, "end_char": 31862, "text_sha256": "8e9b4448f5213862fa4c8b78f1d49c9f6b4e6faffb97d818dabbd4117d386dba"}
experimental_model
High-fat-fed mice and differentiated C2C12 myotube experiments
exposure
200 or 1000 micromolar mangiferin, 15 minutes; Figure 6
limitations
The authors proposed inhibition of kinase activity; this observation alone does not identify a direct molecular target.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
The rapid response differed from the later change in protein abundance.
primary_references
[mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
tissue_or_cell_type
Skeletal muscle and cultured myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 366–377
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-fat-fed mice and differentiated C2C12 myotube experiments · source_derived_draft · unverified_draft
### mangiferin-acute-pdh After 15 minutes, PDH phosphorylation decreased without a detected change in PDK4 abundance. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The rapid response differed from the later change in protein abundance. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and cultured myotubes experimental_model: High-fat-fed mice and differentiated C2C12 myotube experiments limitations: The authors proposed inhibition of kinase activity; this observation alone does not identify a direct molecular target. exposure: 200 or 1000 micromolar mangiferin, 15 minutes; Figure 6 evidence_span: {"source_cache": "artifacts/mangiferin-research/24848064.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cbbc4a9b075ae11f5b88a9929a65c77e6b39870068e320a281bd1802384fec8", "start_char": 30977, "end_char": 31862, "text_sha256": "8e9b4448f5213862fa4c8b78f1d49c9f6b4e6faffb97d818dabbd4117d386dba"} [mangiferin-p24848064] Mangiferin stimulates carbohydrate oxidation and protects against metabolic disorders induced by high-fat diets. (2014). https://pubmed.ncbi.nlm.nih.gov/24848064/ DOI: 10.2337/db14-0006
Complete structured claim and evidence
Mangiferin increased AMPK phosphorylation in L6 myotubes.
Mangiferin → Rat AMP-activated protein kinase complexes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
experimental_model
Normal and insulin-resistant L6 myotube comparison
exposure
Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
limitations
Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The energy-sensing pathway responded in this cell model.
primary_references
[mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
tissue_or_cell_type
L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 379–390
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-mangiferin-ampk Mangiferin increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidence
Norathyriol increased AMPK phosphorylation in L6 myotubes.
Norathyriol → Rat AMP-activated protein kinase complexes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
experimental_model
Normal and insulin-resistant L6 myotube comparison
exposure
Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
limitations
Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The energy-sensing pathway responded in this cell model.
primary_references
[mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
tissue_or_cell_type
L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-norathyriol-ampk Norathyriol increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidence
Mangiferin did not increase Akt phosphorylation in the reported assay.
Mangiferin → Rat L6 myotube Akt phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
experimental_model
Normal and insulin-resistant L6 myotube comparison
exposure
Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
limitations
Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The observed response was not accompanied by this insulin-signaling readout.
primary_references
[mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
tissue_or_cell_type
L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 405–416
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-akt-null Mangiferin did not increase Akt phosphorylation in the reported assay. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The observed response was not accompanied by this insulin-signaling readout. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidence
In insulin-resistant L6 cells, mangiferin increased glucose consumption only with insulin co-treatment; norathyriol worked with or without insulin.
Mangiferin → Rat L6 myotube glucose consumption source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
experimental_model
Normal and insulin-resistant L6 myotube comparison
exposure
Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
limitations
Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The parent compound and metabolite differed under insulin resistance.
primary_references
[mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
tissue_or_cell_type
L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 418–429
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-insulin-context In insulin-resistant L6 cells, mangiferin increased glucose consumption only with insulin co-treatment; norathyriol worked with or without insulin. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The parent compound and metabolite differed under insulin resistance. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidence
Mangiferin and tested metabolites were not direct AMPK activators in the HTRF assay.
Mangiferin → AMPK HTRF assay preparation, subunit and species composition unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d37dba0eedeba51145eddeb7ff144e8f103ec503718283268fe0ae887d6c4125", "start_char": 0, "end_char": 1806, "text_sha256": "d37dba0eedeba51145eddeb7ff144e8f103ec503718283268fe0ae887d6c4125"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
object_scope
Human cellular AMPK context; purified assay subunit identity requires full reagent review
organism
Biochemical AMPK assay, exact subunit preparation not assigned here
plain_language
Activation in a cell can occur through upstream machinery.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 431–443
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-direct-ampk-null Mangiferin and tested metabolites were not direct AMPK activators in the HTRF assay. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activation in a cell can occur through upstream machinery. organism: Biochemical AMPK assay, exact subunit preparation not assigned here tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range object_scope: Human cellular AMPK context; purified assay subunit identity requires full reagent review evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d37dba0eedeba51145eddeb7ff144e8f103ec503718283268fe0ae887d6c4125", "start_char": 0, "end_char": 1806, "text_sha256": "d37dba0eedeba51145eddeb7ff144e8f103ec503718283268fe0ae887d6c4125"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
Norathyriol increased SIRT1 protein expression in HepG2 cells.
Norathyriol → SIRT1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
The metabolite altered an NAD-dependent regulatory pathway.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 445–456
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-sirt1-expression Norathyriol increased SIRT1 protein expression in HepG2 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The metabolite altered an NAD-dependent regulatory pathway. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
Norathyriol lowered measured LKB1 acetylation in HepG2 cells.
Norathyriol → Human LKB1 acetylation in HepG2 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
A chemical modification of an upstream kinase changed.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 458–469
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-lkb1-acetylation Norathyriol lowered measured LKB1 acetylation in HepG2 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemical modification of an upstream kinase changed. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
Norathyriol increased the cellular AMP-to-ATP ratio in the tested HepG2 model.
Norathyriol → AMP-to-ATP ratio in human HepG2 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35775, "end_char": 36269, "text_sha256": "9c428b34591bbbb1e453a4e5e2829b160930ef301d3b39065822f132f5a7dcd9"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
The energy-sensing signal changed alongside AMPK activation.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 471–482
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-energy-ratio Norathyriol increased the cellular AMP-to-ATP ratio in the tested HepG2 model. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing signal changed alongside AMPK activation. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35775, "end_char": 36269, "text_sha256": "9c428b34591bbbb1e453a4e5e2829b160930ef301d3b39065822f132f5a7dcd9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
LKB1 knockdown blocked the triglyceride-lowering response to norathyriol.
Experimental human STK11 / LKB1 siRNA knockdown → Triglyceride accumulation in human HepG2 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
Removing an upstream component interrupted the response.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 484–495
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-lkb1-tg LKB1 knockdown blocked the triglyceride-lowering response to norathyriol. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation.
Experimental human STK11 / LKB1 siRNA knockdown → Human acetyl-CoA carboxylase activity, isoform unresolved in assay source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
experimental_model
KK-Ay mouse liver experiments and mechanistic HepG2 studies
exposure
Norathyriol in sodium-oleate lipid-loading model; micromolar range
limitations
Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens for HepG2 experiments; mouse findings separately scoped
plain_language
Removing an upstream component interrupted the response.
primary_references
[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
tissue_or_cell_type
HepG2 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 510–521
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft
### mangiferin-lkb1-acc LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
Complete structured claim and evidence
Nrf2 half-life increased from 20 to 58 minutes in the HL-60 chase experiment.
Mangiferin → Nrf2 protein stability source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"}
experimental_model
Cycloheximide chase and immunoprecipitation
exposure
Mangiferin 50 micromolar for four hours in half-life experiment
limitations
Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
The protein persisted longer before degradation.
primary_references
[mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
tissue_or_cell_type
HL-60 myeloid leukemia cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 523–534
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cycloheximide chase and immunoprecipitation · source_derived_draft · unverified_draft
### mangiferin-nrf2-half-life Nrf2 half-life increased from 20 to 58 minutes in the HL-60 chase experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein persisted longer before degradation. organism: Homo sapiens tissue_or_cell_type: HL-60 myeloid leukemia cells experimental_model: Cycloheximide chase and immunoprecipitation limitations: Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference. exposure: Mangiferin 50 micromolar for four hours in half-life experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"} [mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
Complete structured claim and evidence
Immunoprecipitation showed reduced Nrf2 ubiquitination after mangiferin treatment.
Mangiferin → Nrf2 ubiquitination in human HL-60 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"}
experimental_model
Cycloheximide chase and immunoprecipitation
exposure
Mangiferin 50 micromolar for four hours in half-life experiment
limitations
Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
Less degradation-associated tagging was detected.
primary_references
[mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
tissue_or_cell_type
HL-60 myeloid leukemia cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 536–547
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cycloheximide chase and immunoprecipitation · source_derived_draft · unverified_draft
### mangiferin-nrf2-ubiquitination Immunoprecipitation showed reduced Nrf2 ubiquitination after mangiferin treatment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less degradation-associated tagging was detected. organism: Homo sapiens tissue_or_cell_type: HL-60 myeloid leukemia cells experimental_model: Cycloheximide chase and immunoprecipitation limitations: Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference. exposure: Mangiferin 50 micromolar for four hours in half-life experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"} [mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
Complete structured claim and evidence
Mangiferin did not change the Nrf2 mRNA level in this study.
Mangiferin → Human NFE2L2 transcript abundance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"}
experimental_model
Cycloheximide chase and immunoprecipitation
exposure
Mangiferin 50 micromolar for four hours in half-life experiment
limitations
Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
The protein increase did not require more measured transcript.
primary_references
[mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
tissue_or_cell_type
HL-60 myeloid leukemia cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 549–560
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cycloheximide chase and immunoprecipitation · source_derived_draft · unverified_draft
### mangiferin-nrf2-transcript-null Mangiferin did not change the Nrf2 mRNA level in this study. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein increase did not require more measured transcript. organism: Homo sapiens tissue_or_cell_type: HL-60 myeloid leukemia cells experimental_model: Cycloheximide chase and immunoprecipitation limitations: Cancer cell line; no direct KEAP1-binding assignment or human systemic target-engagement inference. exposure: Mangiferin 50 micromolar for four hours in half-life experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/24626801.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd", "start_char": 0, "end_char": 1659, "text_sha256": "01992b219c903dddc6e69f5fef95f73cec06cdaac0fd2c5bc2ff7b53b52192cd"} [mangiferin-p24626801] Mangiferin increases Nrf2 protein stability by inhibiting its ubiquitination and degradation in human HL60 myeloid leukemia cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24626801/ DOI: 10.3892/ijmm.2014.1696
Complete structured claim and evidence
Mangiferin increased nuclear Nrf2 accumulation.
Mangiferin → Human Nrf2 nuclear accumulation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"}
experimental_model
Isolated human cord-blood mononuclear cells
exposure
Mangiferin and etoposide; concentration not specified in indexed abstract
limitations
Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
More of the regulator reached the nuclear compartment.
primary_references
[mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
tissue_or_cell_type
Cord-blood mononuclear cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 562–573
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human cord-blood mononuclear cells · source_derived_draft · unverified_draft
### mangiferin-nrf2-nuclear Mangiferin increased nuclear Nrf2 accumulation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More of the regulator reached the nuclear compartment. organism: Homo sapiens tissue_or_cell_type: Cord-blood mononuclear cells experimental_model: Isolated human cord-blood mononuclear cells limitations: Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection. exposure: Mangiferin and etoposide; concentration not specified in indexed abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"} [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
Complete structured claim and evidence
Mangiferin increased NQO1 expression in cord-blood mononuclear cells.
Mangiferin → Human NAD(P)H quinone dehydrogenase 1 / NQO1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"}
experimental_model
Isolated human cord-blood mononuclear cells
exposure
Mangiferin and etoposide; concentration not specified in indexed abstract
limitations
Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A quinone-processing defense enzyme responded.
primary_references
[mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
tissue_or_cell_type
Cord-blood mononuclear cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 575–586
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human cord-blood mononuclear cells · source_derived_draft · unverified_draft
### mangiferin-nqo1 Mangiferin increased NQO1 expression in cord-blood mononuclear cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A quinone-processing defense enzyme responded. organism: Homo sapiens tissue_or_cell_type: Cord-blood mononuclear cells experimental_model: Isolated human cord-blood mononuclear cells limitations: Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection. exposure: Mangiferin and etoposide; concentration not specified in indexed abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"} [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
Complete structured claim and evidence
Mangiferin reduced etoposide-associated comet and micronucleus damage readouts.
Mangiferin → Etoposide-associated DNA damage in human cord-blood mononuclear cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"}
experimental_model
Isolated human cord-blood mononuclear cells
exposure
Mangiferin and etoposide; concentration not specified in indexed abstract
limitations
Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
DNA-damage measurements were lower in these isolated cells.
primary_references
[mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
tissue_or_cell_type
Cord-blood mononuclear cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 588–599
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human cord-blood mononuclear cells · source_derived_draft · unverified_draft
### mangiferin-dna-damage Mangiferin reduced etoposide-associated comet and micronucleus damage readouts. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: DNA-damage measurements were lower in these isolated cells. organism: Homo sapiens tissue_or_cell_type: Cord-blood mononuclear cells experimental_model: Isolated human cord-blood mononuclear cells limitations: Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection. exposure: Mangiferin and etoposide; concentration not specified in indexed abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"} [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
Complete structured claim and evidence
Mangiferin preserved the glutathione pool during H2O2 exposure.
Mangiferin → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
experimental_model
Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
exposure
Mangiferin before H2O2 exposure
limitations
Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A cellular redox buffer was better maintained.
primary_references
[mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
tissue_or_cell_type
ARPE-19 retinal pigment epithelial cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 601–612
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft
### mangiferin-rpe-gsh Mangiferin preserved the glutathione pool during H2O2 exposure. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cellular redox buffer was better maintained. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
Complete structured claim and evidence
Mangiferin opposed H2O2-associated loss of glutathione peroxidase expression and activity.
Mangiferin → Human glutathione peroxidase activity, isoform unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
experimental_model
Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
exposure
Mangiferin before H2O2 exposure
limitations
Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
Peroxide-processing enzyme activity was preserved; the isoform remains unspecified.
primary_references
[mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
tissue_or_cell_type
ARPE-19 retinal pigment epithelial cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 627–638
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft
### mangiferin-rpe-gpx Mangiferin opposed H2O2-associated loss of glutathione peroxidase expression and activity. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Peroxide-processing enzyme activity was preserved; the isoform remains unspecified. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
Complete structured claim and evidence
Mangiferin increased HO-1 expression and activity in ARPE-19 cells.
Mangiferin → Human heme oxygenase 1 / HMOX1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
experimental_model
Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
exposure
Mangiferin before H2O2 exposure
limitations
Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
The heme-processing stress-response pathway was activated.
primary_references
[mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
tissue_or_cell_type
ARPE-19 retinal pigment epithelial cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 640–651
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft
### mangiferin-rpe-ho1 Mangiferin increased HO-1 expression and activity in ARPE-19 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The heme-processing stress-response pathway was activated. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
Complete structured claim and evidence
HO-1 inhibition attenuated the protective effect of mangiferin against H2O2 injury.
Experimental HO-1 inhibitor exposure → Hydrogen-peroxide injury in human ARPE-19 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
experimental_model
Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
exposure
Mangiferin before H2O2 exposure
limitations
Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
The response depended in part on available enzyme activity.
primary_references
[mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
tissue_or_cell_type
ARPE-19 retinal pigment epithelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 653–664
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft
### mangiferin-ho1-loss HO-1 inhibition attenuated the protective effect of mangiferin against H2O2 injury. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response depended in part on available enzyme activity. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
Complete structured claim and evidence
Mangiferin inhibited ferrous-citrate-triggered mitochondrial lipid peroxidation.
Mangiferin → Rat liver mitochondrial lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"}
experimental_model
Isolated mitochondrial and iron-redox assays
exposure
10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment
limitations
In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
Binding iron altered its ability to drive membrane oxidation.
primary_references
[mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
tissue_or_cell_type
Liver mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 666–677
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated mitochondrial and iron-redox assays · source_derived_draft · unverified_draft
### mangiferin-iron-lipid Mangiferin inhibited ferrous-citrate-triggered mitochondrial lipid peroxidation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Binding iron altered its ability to drive membrane oxidation. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Liver mitochondria experimental_model: Isolated mitochondrial and iron-redox assays limitations: In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload. exposure: 10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"} [mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
Complete structured claim and evidence
Mangiferin accelerated ferrous iron autoxidation in the tested system.
Mangiferin → Ferrous iron autoxidation in vitro source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"}
experimental_model
Isolated mitochondrial and iron-redox assays
exposure
10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment
limitations
In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
The iron oxidation state shifted.
primary_references
[mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
tissue_or_cell_type
Liver mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 679–690
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated mitochondrial and iron-redox assays · source_derived_draft · unverified_draft
### mangiferin-iron-oxidation Mangiferin accelerated ferrous iron autoxidation in the tested system. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The iron oxidation state shifted. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Liver mitochondria experimental_model: Isolated mitochondrial and iron-redox assays limitations: In vitro iron complexing is not evidence that oral mangiferin depletes body iron or treats iron overload. exposure: 10 micromolar mangiferin and 50 micromolar ferrous citrate in one protection experiment evidence_span: {"source_cache": "artifacts/mangiferin-research/15878708.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3", "start_char": 0, "end_char": 1966, "text_sha256": "e29d024822df85f1aa0b737bb4123c869646d737c15bf05f1dc72b047a45eef3"} [mangiferin-p15878708] Iron complexing activity of mangiferin, a naturally occurring glucosylxanthone, inhibits mitochondrial lipid peroxidation induced by Fe2+-citrate. (2005). https://pubmed.ncbi.nlm.nih.gov/15878708/ DOI: 10.1016/j.ejphar.2005.03.007
Complete structured claim and evidence
Calcium-challenged mitochondria from treated rats showed glutathione depletion.
Mangiferin → Rat liver mitochondrial glutathione oxidation or depletion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/15979560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f", "start_char": 0, "end_char": 2234, "text_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f"}
experimental_model
Rat pretreatment and isolated mitochondrial calcium challenge
exposure
40 mg/kg mangiferin pretreatment; isolated mitochondria exposed to calcium
limitations
Mitochondrial challenge does not establish harm from usual oral intake; proposed quinone-thiol adduct mechanism was not fully proven.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus
plain_language
The calcium challenge changed the redox consequences.
primary_references
[mangiferin-p15979560] Mangiferin, a natural occurring glucosyl xanthone, increases susceptibility of rat liver mitochondria to calcium-induced permeability transition. (2005). https://pubmed.ncbi.nlm.nih.gov/15979560/ DOI: 10.1016/j.abb.2005.05.015
tissue_or_cell_type
Liver mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 718–729
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pretreatment and isolated mitochondrial calcium challenge · source_derived_draft · unverified_draft
### mangiferin-calcium-gsh Calcium-challenged mitochondria from treated rats showed glutathione depletion. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium challenge changed the redox consequences. organism: Rattus norvegicus tissue_or_cell_type: Liver mitochondria experimental_model: Rat pretreatment and isolated mitochondrial calcium challenge limitations: Mitochondrial challenge does not establish harm from usual oral intake; proposed quinone-thiol adduct mechanism was not fully proven. exposure: 40 mg/kg mangiferin pretreatment; isolated mitochondria exposed to calcium evidence_span: {"source_cache": "artifacts/mangiferin-research/15979560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f", "start_char": 0, "end_char": 2234, "text_sha256": "3de89f65f9561fd94c5f07121e8150f116c59277658d7e611a399dc2d963ec1f"} [mangiferin-p15979560] Mangiferin, a natural occurring glucosyl xanthone, increases susceptibility of rat liver mitochondria to calcium-induced permeability transition. (2005). https://pubmed.ncbi.nlm.nih.gov/15979560/ DOI: 10.1016/j.abb.2005.05.015
Complete structured claim and evidence
Electrochemical and spectroscopic analyses supported coordination of ferric iron with mangiferin.
Mangiferin → Mangiferin-ferric iron complex, assay-defined source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"}
experimental_model
Iron-coordination spectroscopy and mitochondrial challenge
exposure
Assay-defined ferric iron-mangiferin complex
limitations
Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
The metal-bound form is represented separately.
primary_references
[mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
tissue_or_cell_type
Isolated mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 731–742
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Iron-coordination spectroscopy and mitochondrial challenge · source_derived_draft · unverified_draft
### mangiferin-ferric-complex Electrochemical and spectroscopic analyses supported coordination of ferric iron with mangiferin. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The metal-bound form is represented separately. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Isolated mitochondria experimental_model: Iron-coordination spectroscopy and mitochondrial challenge limitations: Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation. exposure: Assay-defined ferric iron-mangiferin complex evidence_span: {"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"} [mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
Complete structured claim and evidence
The ferric complex protected mitochondrial glutathione against oxidation.
Mangiferin-ferric iron complex, assay-defined → Rat liver mitochondrial glutathione oxidation or depletion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"}
experimental_model
Iron-coordination spectroscopy and mitochondrial challenge
exposure
Assay-defined ferric iron-mangiferin complex
limitations
Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus and cell-free chemistry
plain_language
Metal coordination altered protection of the redox buffer.
primary_references
[mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
tissue_or_cell_type
Isolated mitochondria
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 757–768
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Iron-coordination spectroscopy and mitochondrial challenge · source_derived_draft · unverified_draft
### mangiferin-complex-gsh The ferric complex protected mitochondrial glutathione against oxidation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Metal coordination altered protection of the redox buffer. organism: Rattus norvegicus and cell-free chemistry tissue_or_cell_type: Isolated mitochondria experimental_model: Iron-coordination spectroscopy and mitochondrial challenge limitations: Defined chemical form and calcium context explain the different response; no clinical iron/mangiferin co-dosing recommendation. exposure: Assay-defined ferric iron-mangiferin complex evidence_span: {"source_cache": "artifacts/mangiferin-research/17068204.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64", "start_char": 0, "end_char": 1172, "text_sha256": "1d0b364cee6629228fe7bc41446a0e2ddfe62b9274d77d4781ca7439aedfbb64"} [mangiferin-p17068204] Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle. (2007). https://pubmed.ncbi.nlm.nih.gov/17068204/ DOI: 10.1124/jpet.106.112003
Complete structured claim and evidence
Mangiferin reduced measured CYP1A2 activity in the hepatocyte experiment.
Mangiferin → Human cytochrome P450 1A2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A drug-metabolizing enzyme was inhibited under the tested exposure.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 770–781
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-cyp1a2-activity Mangiferin reduced measured CYP1A2 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
Mangiferin reduced measured CYP2A6 activity in the hepatocyte experiment.
Mangiferin → Human cytochrome P450 2A6 / CYP2A6 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A drug-metabolizing enzyme was inhibited under the tested exposure.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 783–794
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-cyp2a6-activity Mangiferin reduced measured CYP2A6 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
Mangiferin reduced measured CYP2C9 activity in the hepatocyte experiment.
Mangiferin → Human cytochrome P450 2C9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A drug-metabolizing enzyme was inhibited under the tested exposure.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 796–807
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-cyp2c9-activity Mangiferin reduced measured CYP2C9 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
Mangiferin reduced measured CYP2D6 activity in the hepatocyte experiment.
Mangiferin → Human cytochrome P450 2D6 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A drug-metabolizing enzyme was inhibited under the tested exposure.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 809–820
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-cyp2d6-activity Mangiferin reduced measured CYP2D6 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
Mangiferin reduced measured CYP3A4 activity in the hepatocyte experiment.
Mangiferin → Human cytochrome P450 3A4 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A drug-metabolizing enzyme was inhibited under the tested exposure.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 822–833
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-cyp3a4-activity Mangiferin reduced measured CYP3A4 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
At 250 micrograms/mL, mangiferin reduced UGT1A1 activity by about 55 percent.
Mangiferin → Human UDP-glucuronosyltransferase 1A1 / UGT1A1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A conjugation pathway also responded in vitro.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 835–846
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-ugt1a1-activity At 250 micrograms/mL, mangiferin reduced UGT1A1 activity by about 55 percent. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A conjugation pathway also responded in vitro. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
At 250 micrograms/mL, mangiferin reduced UGT2B7 activity by about 55 percent.
Mangiferin → Human UDP-glucuronosyltransferase 2B7 / UGT2B7 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A conjugation pathway also responded in vitro.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 848–859
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-ugt2b7-activity At 250 micrograms/mL, mangiferin reduced UGT2B7 activity by about 55 percent. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A conjugation pathway also responded in vitro. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
At 250 micrograms/mL, mangiferin reduced UGT1A9 activity by about 35 percent.
Mangiferin → Human UDP-glucuronosyltransferase 1A9 / UGT1A9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}
experimental_model
Primary human hepatocyte exposure
exposure
Mangiferin 50-250 micrograms/mL for 48 hours
limitations
High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A conjugation pathway also responded in vitro.
primary_references
[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
tissue_or_cell_type
Cultured hepatocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 861–872
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft
### mangiferin-ugt1a9-activity At 250 micrograms/mL, mangiferin reduced UGT1A9 activity by about 35 percent. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A conjugation pathway also responded in vitro. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782
Complete structured claim and evidence
Norathyriol competitively inhibited UGT1A3; IC50 8.2 and Ki 1.6 micromolar.
Norathyriol → Human UDP-glucuronosyltransferase 1A3 / UGT1A3 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"}
experimental_model
Recombinant UGT inhibition kinetics
exposure
Micromolar norathyriol; initial comparison at 100 micromolar
limitations
Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Recombinant enzyme assay
plain_language
The aglycone has its own conjugation-enzyme interaction profile.
primary_references
[mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
tissue_or_cell_type
4-methylumbelliferone glucuronidation
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 874–885
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant UGT inhibition kinetics · source_derived_draft · unverified_draft
### mangiferin-norathyriol-ugt1a3 Norathyriol competitively inhibited UGT1A3; IC50 8.2 and Ki 1.6 micromolar. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The aglycone has its own conjugation-enzyme interaction profile. organism: Recombinant enzyme assay tissue_or_cell_type: 4-methylumbelliferone glucuronidation experimental_model: Recombinant UGT inhibition kinetics limitations: Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo. exposure: Micromolar norathyriol; initial comparison at 100 micromolar evidence_span: {"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"} [mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
Complete structured claim and evidence
Norathyriol competitively inhibited UGT1A7; IC50 4.4 and Ki 2.0 micromolar.
Norathyriol → Human UDP-glucuronosyltransferase 1A7 / UGT1A7 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"}
experimental_model
Recombinant UGT inhibition kinetics
exposure
Micromolar norathyriol; initial comparison at 100 micromolar
limitations
Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Recombinant enzyme assay
plain_language
The aglycone has its own conjugation-enzyme interaction profile.
primary_references
[mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
tissue_or_cell_type
4-methylumbelliferone glucuronidation
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 887–898
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant UGT inhibition kinetics · source_derived_draft · unverified_draft
### mangiferin-norathyriol-ugt1a7 Norathyriol competitively inhibited UGT1A7; IC50 4.4 and Ki 2.0 micromolar. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The aglycone has its own conjugation-enzyme interaction profile. organism: Recombinant enzyme assay tissue_or_cell_type: 4-methylumbelliferone glucuronidation experimental_model: Recombinant UGT inhibition kinetics limitations: Probe-dependent biochemical inhibition; no established human interaction threshold. Docking is not additional proof of binding in vivo. exposure: Micromolar norathyriol; initial comparison at 100 micromolar evidence_span: {"source_cache": "artifacts/mangiferin-research/28621744.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5", "start_char": 0, "end_char": 1562, "text_sha256": "e2741f9036a84104809f4d9813afeb1603b3e93e1d247ea0e4b5ff31be0e1ae5"} [mangiferin-p28621744] In Vitro Comparative Study of the Inhibitory Effects of Mangiferin and Its Aglycone Norathyriol towards UDP-Glucuronosyl Transferase (UGT) Isoforms. (2017). https://pubmed.ncbi.nlm.nih.gov/28621744/ DOI: 10.3390/molecules22061008
Complete structured claim and evidence
Mangiferin reduced renal Rat urate transporter 1 / Slc22a12 mRNA and protein in hyperuricemic rats.
Mangiferin → Rat urate transporter 1 / Slc22a12 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"}
experimental_model
Experimental hyperuricemia in rodents
exposure
Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model
limitations
Abundance changes do not prove direct transporter blockade or clinical gout efficacy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus for transporter findings
plain_language
Less of a urate-reabsorption transporter was measured.
primary_references
[mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 913–924
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental hyperuricemia in rodents · source_derived_draft · unverified_draft
### mangiferin-rat-slc22a12 Mangiferin reduced renal Rat urate transporter 1 / Slc22a12 mRNA and protein in hyperuricemic rats. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less of a urate-reabsorption transporter was measured. organism: Rattus norvegicus for transporter findings tissue_or_cell_type: Kidney experimental_model: Experimental hyperuricemia in rodents limitations: Abundance changes do not prove direct transporter blockade or clinical gout efficacy. exposure: Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model evidence_span: {"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"} [mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
Complete structured claim and evidence
Mangiferin reduced renal Rat organic anion transporter 10 / Slc22a13 mRNA and protein in hyperuricemic rats.
Mangiferin → Rat organic anion transporter 10 / Slc22a13 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"}
experimental_model
Experimental hyperuricemia in rodents
exposure
Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model
limitations
Abundance changes do not prove direct transporter blockade or clinical gout efficacy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus for transporter findings
plain_language
Less of a urate-reabsorption transporter was measured.
primary_references
[mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 926–937
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental hyperuricemia in rodents · source_derived_draft · unverified_draft
### mangiferin-rat-slc22a13 Mangiferin reduced renal Rat organic anion transporter 10 / Slc22a13 mRNA and protein in hyperuricemic rats. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less of a urate-reabsorption transporter was measured. organism: Rattus norvegicus for transporter findings tissue_or_cell_type: Kidney experimental_model: Experimental hyperuricemia in rodents limitations: Abundance changes do not prove direct transporter blockade or clinical gout efficacy. exposure: Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model evidence_span: {"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"} [mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
Complete structured claim and evidence
Mangiferin reduced renal Rat glucose transporter 9 / Slc2a9 mRNA and protein in hyperuricemic rats.
Mangiferin → Rat glucose transporter 9 / Slc2a9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"}
experimental_model
Experimental hyperuricemia in rodents
exposure
Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model
limitations
Abundance changes do not prove direct transporter blockade or clinical gout efficacy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus for transporter findings
plain_language
Less of a urate-reabsorption transporter was measured.
primary_references
[mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 939–950
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental hyperuricemia in rodents · source_derived_draft · unverified_draft
### mangiferin-rat-slc2a9 Mangiferin reduced renal Rat glucose transporter 9 / Slc2a9 mRNA and protein in hyperuricemic rats. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less of a urate-reabsorption transporter was measured. organism: Rattus norvegicus for transporter findings tissue_or_cell_type: Kidney experimental_model: Experimental hyperuricemia in rodents limitations: Abundance changes do not prove direct transporter blockade or clinical gout efficacy. exposure: Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model evidence_span: {"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"} [mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
Complete structured claim and evidence
Renal PDZK1 expression was not altered in the same rat experiment.
Mangiferin → Rat PDZK1 scaffold protein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"}
experimental_model
Experimental hyperuricemia in rodents
exposure
Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model
limitations
Abundance changes do not prove direct transporter blockade or clinical gout efficacy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Rattus norvegicus for transporter findings
plain_language
The response did not include every related transport component.
primary_references
[mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 952–963
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental hyperuricemia in rodents · source_derived_draft · unverified_draft
### mangiferin-pdzk1-null Renal PDZK1 expression was not altered in the same rat experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response did not include every related transport component. organism: Rattus norvegicus for transporter findings tissue_or_cell_type: Kidney experimental_model: Experimental hyperuricemia in rodents limitations: Abundance changes do not prove direct transporter blockade or clinical gout efficacy. exposure: Mangiferin 1.5-24 mg/kg; potassium-oxonate rat model evidence_span: {"source_cache": "artifacts/mangiferin-research/26228630.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c", "start_char": 0, "end_char": 1633, "text_sha256": "d7d497620fe96b2161af66b3d58b0a4ef8208f10f6d669fc680b85aa38b8d85c"} [mangiferin-p26228630] Mangiferin Inhibits Renal Urate Reabsorption by Modulating Urate Transporters in Experimental Hyperuricemia. (2015). https://pubmed.ncbi.nlm.nih.gov/26228630/ DOI: 10.1248/bpb.b15-00402
Complete structured claim and evidence
Mangiferin reduced renal Mouse urate transporter 1 / Slc22a12 expression in the hyperuricemic mice.
Mangiferin → Mouse urate transporter 1 / Slc22a12 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"}
experimental_model
Seven-day potassium-oxonate hyperuricemia model
exposure
Mangiferin 50, 100 or 200 mg/kg orally
limitations
Animal expression findings; no human carnitine-retention or gout-treatment conclusion.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
Urate-reabsorption machinery changed.
primary_references
[mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 965–976
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven-day potassium-oxonate hyperuricemia model · source_derived_draft · unverified_draft
### mangiferin-mouse-slc22a12 Mangiferin reduced renal Mouse urate transporter 1 / Slc22a12 expression in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urate-reabsorption machinery changed. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Seven-day potassium-oxonate hyperuricemia model limitations: Animal expression findings; no human carnitine-retention or gout-treatment conclusion. exposure: Mangiferin 50, 100 or 200 mg/kg orally evidence_span: {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"} [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
Complete structured claim and evidence
Mangiferin reduced renal Mouse glucose transporter 9 / Slc2a9 expression in the hyperuricemic mice.
Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"}
experimental_model
Seven-day potassium-oxonate hyperuricemia model
exposure
Mangiferin 50, 100 or 200 mg/kg orally
limitations
Animal expression findings; no human carnitine-retention or gout-treatment conclusion.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
Another urate transporter responded.
primary_references
[mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 978–989
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven-day potassium-oxonate hyperuricemia model · source_derived_draft · unverified_draft
### mangiferin-mouse-slc2a9 Mangiferin reduced renal Mouse glucose transporter 9 / Slc2a9 expression in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another urate transporter responded. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Seven-day potassium-oxonate hyperuricemia model limitations: Animal expression findings; no human carnitine-retention or gout-treatment conclusion. exposure: Mangiferin 50, 100 or 200 mg/kg orally evidence_span: {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"} [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
Complete structured claim and evidence
Mangiferin increased renal Mouse organic anion transporter 1 / Slc22a6 expression in the hyperuricemic mice.
Mangiferin → Mouse organic anion transporter 1 / Slc22a6 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"}
experimental_model
Seven-day potassium-oxonate hyperuricemia model
exposure
Mangiferin 50, 100 or 200 mg/kg orally
limitations
Animal expression findings; no human carnitine-retention or gout-treatment conclusion.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
An organic-anion transport route increased.
primary_references
[mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 991–1002
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven-day potassium-oxonate hyperuricemia model · source_derived_draft · unverified_draft
### mangiferin-mouse-slc22a6 Mangiferin increased renal Mouse organic anion transporter 1 / Slc22a6 expression in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An organic-anion transport route increased. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Seven-day potassium-oxonate hyperuricemia model limitations: Animal expression findings; no human carnitine-retention or gout-treatment conclusion. exposure: Mangiferin 50, 100 or 200 mg/kg orally evidence_span: {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"} [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
Complete structured claim and evidence
Mangiferin increased renal Mouse carnitine transporter Octn2 / Slc22a5 expression in the hyperuricemic mice.
Mangiferin → Mouse carnitine transporter Octn2 / Slc22a5 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"}
experimental_model
Seven-day potassium-oxonate hyperuricemia model
exposure
Mangiferin 50, 100 or 200 mg/kg orally
limitations
Animal expression findings; no human carnitine-retention or gout-treatment conclusion.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
A transporter linked to carnitine also responded.
primary_references
[mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
tissue_or_cell_type
Kidney
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1004–1015
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven-day potassium-oxonate hyperuricemia model · source_derived_draft · unverified_draft
### mangiferin-mouse-slc22a5 Mangiferin increased renal Mouse carnitine transporter Octn2 / Slc22a5 expression in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter linked to carnitine also responded. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Seven-day potassium-oxonate hyperuricemia model limitations: Animal expression findings; no human carnitine-retention or gout-treatment conclusion. exposure: Mangiferin 50, 100 or 200 mg/kg orally evidence_span: {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"} [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
Complete structured claim and evidence
Mangiferin reduced renal AQP2 protein expression in nephropathy mice.
Mangiferin → Mouse aquaporin 2 / Aqp2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
experimental_model
Mouse hyperuricemic nephropathy experiment
exposure
Mangiferin in the study-specific nephropathy model
limitations
Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
Water-handling machinery changed in this model.
primary_references
[mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
tissue_or_cell_type
Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1017–1028
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-aqp2 Mangiferin reduced renal AQP2 protein expression in nephropathy mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Water-handling machinery changed in this model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidence
Urine volume increased without a marked change in urine urate concentration.
Mangiferin → Mouse urine output source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
experimental_model
Mouse hyperuricemic nephropathy experiment
exposure
Mangiferin in the study-specific nephropathy model
limitations
Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
More urate could leave through greater urine output.
primary_references
[mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
tissue_or_cell_type
Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1030–1041
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-urine-output Urine volume increased without a marked change in urine urate concentration. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More urate could leave through greater urine output. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidence
No change in renal Mouse urate transporter 1 / Slc22a12 expression was detected in the nephropathy model.
Mangiferin → Mouse urate transporter 1 / Slc22a12 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
experimental_model
Mouse hyperuricemic nephropathy experiment
exposure
Mangiferin in the study-specific nephropathy model
limitations
Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
This transport-protein response differed from the earlier hyperuricemia model.
primary_references
[mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
tissue_or_cell_type
Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1043–1054
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-mouse-slc22a12-null No change in renal Mouse urate transporter 1 / Slc22a12 expression was detected in the nephropathy model. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This transport-protein response differed from the earlier hyperuricemia model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidence
No change in renal Mouse glucose transporter 9 / Slc2a9 expression was detected in the nephropathy model.
Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
experimental_model
Mouse hyperuricemic nephropathy experiment
exposure
Mangiferin in the study-specific nephropathy model
limitations
Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
This transport-protein response differed from the earlier hyperuricemia model.
primary_references
[mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
tissue_or_cell_type
Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1056–1067
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-mouse-slc2a9-null No change in renal Mouse glucose transporter 9 / Slc2a9 expression was detected in the nephropathy model. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This transport-protein response differed from the earlier hyperuricemia model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidence
No change in renal Mouse organic anion transporter 1 / Slc22a6 expression was detected in the nephropathy model.
Mangiferin → Mouse organic anion transporter 1 / Slc22a6 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
experimental_model
Mouse hyperuricemic nephropathy experiment
exposure
Mangiferin in the study-specific nephropathy model
limitations
Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mus musculus
plain_language
This transport-protein response differed from the earlier hyperuricemia model.
primary_references
[mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
tissue_or_cell_type
Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1069–1080
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-mouse-slc22a6-null No change in renal Mouse organic anion transporter 1 / Slc22a6 expression was detected in the nephropathy model. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This transport-protein response differed from the earlier hyperuricemia model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidence
Mangiferin promoted endogenous urate secretion into mouse intestinal loops.
Mangiferin → Mouse intestinal urate secretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
experimental_model
Rodent intestinal-loop secretion/absorption experiments
exposure
Mangiferin in normal and hyperuricemic loop experiments
limitations
Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mice for secretion/proteins; rats for absorption
plain_language
The intestine is another measured route of urate elimination.
primary_references
[mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
tissue_or_cell_type
Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1082–1093
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-secretion Mangiferin promoted endogenous urate secretion into mouse intestinal loops. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestine is another measured route of urate elimination. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Mangiferin inhibited absorption of perfused urate from rat intestinal loops.
Mangiferin → Rat intestinal urate absorption source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
experimental_model
Rodent intestinal-loop secretion/absorption experiments
exposure
Mangiferin in normal and hyperuricemic loop experiments
limitations
Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mice for secretion/proteins; rats for absorption
plain_language
Less of the administered urate crossed back from the gut.
primary_references
[mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
tissue_or_cell_type
Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1095–1106
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-absorption Mangiferin inhibited absorption of perfused urate from rat intestinal loops. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less of the administered urate crossed back from the gut. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Intestinal ABCG2 protein increased in mangiferin-treated hyperuricemic mice.
Mangiferin → Mouse Abcg2 / Bcrp1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
experimental_model
Rodent intestinal-loop secretion/absorption experiments
exposure
Mangiferin in normal and hyperuricemic loop experiments
limitations
Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mice for secretion/proteins; rats for absorption
plain_language
A shared drug and metabolite transporter changed in this tissue.
primary_references
[mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
tissue_or_cell_type
Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1108–1119
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-abcg2 Intestinal ABCG2 protein increased in mangiferin-treated hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shared drug and metabolite transporter changed in this tissue. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Intestinal GLUT9 protein decreased in the hyperuricemic mice.
Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
experimental_model
Rodent intestinal-loop secretion/absorption experiments
exposure
Mangiferin in normal and hyperuricemic loop experiments
limitations
Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mice for secretion/proteins; rats for absorption
plain_language
Another intestinal urate route changed in the opposite direction.
primary_references
[mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
tissue_or_cell_type
Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1121–1132
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-glut9 Intestinal GLUT9 protein decreased in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another intestinal urate route changed in the opposite direction. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Intestinal xanthine oxidoreductase activity did not change significantly.
Mangiferin → Mouse intestinal xanthine oxidoreductase activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
experimental_model
Rodent intestinal-loop secretion/absorption experiments
exposure
Mangiferin in normal and hyperuricemic loop experiments
limitations
Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Mice for secretion/proteins; rats for absorption
plain_language
Reduced blood urate need not reflect lower intestinal urate synthesis.
primary_references
[mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
tissue_or_cell_type
Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1134–1145
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-xor-null Intestinal xanthine oxidoreductase activity did not change significantly. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced blood urate need not reflect lower intestinal urate synthesis. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Serum free fatty acids decreased compared with placebo.
Mangiferin → Human serum free fatty acid concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
Another circulating lipid measure changed.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1160–1171
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-ffa Serum free fatty acids decreased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another circulating lipid measure changed. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
HOMA-IR decreased compared with placebo.
Mangiferin → HOMA-IR estimate of insulin resistance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
An estimated insulin-resistance index improved.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1173–1184
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-homa HOMA-IR decreased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An estimated insulin-resistance index improved. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
HDL cholesterol increased compared with placebo.
Mangiferin → HDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
The measured lipoprotein profile changed.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1186–1197
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-hdl HDL cholesterol increased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured lipoprotein profile changed. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Serum beta-hydroxybutyrate increased compared with placebo.
Mangiferin → Human serum beta-hydroxybutyrate concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
A circulating ketone measure increased.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1212–1223
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-bhb Serum beta-hydroxybutyrate increased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A circulating ketone measure increased. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Serum acetoacetate increased compared with placebo.
Mangiferin → Human serum acetoacetate concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
A second ketone measure increased.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1225–1236
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-acetoacetate Serum acetoacetate increased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second ketone measure increased. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Lipoprotein lipase activity increased compared with placebo.
Mangiferin → Human circulating lipoprotein lipase activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
Measured lipid-processing enzyme activity increased.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1238–1249
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-lpl Lipoprotein lipase activity increased compared with placebo. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Measured lipid-processing enzyme activity increased. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Serum insulin did not differ significantly between groups.
Mangiferin → Human serum insulin concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
A changed index does not mean each component changed significantly.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1264–1275
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-insulin-null Serum insulin did not differ significantly between groups. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A changed index does not mean each component changed significantly. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
LDL cholesterol did not differ significantly between groups.
Mangiferin → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
The result does not support an across-the-board cholesterol claim.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1277–1288
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-ldl-null LDL cholesterol did not differ significantly between groups. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The result does not support an across-the-board cholesterol claim. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Total cholesterol did not differ significantly between groups.
Mangiferin → Human serum total cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"}
experimental_model
Double-blind randomized placebo-controlled trial
exposure
Mangiferin 150 mg/day for 12 weeks
limitations
One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Overweight adults with hyperlipidemia; 97 completers
plain_language
This cholesterol endpoint was also unchanged.
primary_references
[mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
tissue_or_cell_type
Serum metabolic measurements
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1290–1301
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### mangiferin-trial-total-chol-null Total cholesterol did not differ significantly between groups. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This cholesterol endpoint was also unchanged. organism: Overweight adults with hyperlipidemia; 97 completers tissue_or_cell_type: Serum metabolic measurements experimental_model: Double-blind randomized placebo-controlled trial limitations: One trial in a selected population; biomarkers do not demonstrate clinical outcomes or directly measure fatty-acid flux. exposure: Mangiferin 150 mg/day for 12 weeks evidence_span: {"source_cache": "artifacts/mangiferin-research/25989216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539", "start_char": 0, "end_char": 1522, "text_sha256": "2f57445ffe1eb20de3c2bf1170d152c358be1d7763cef2a091c0b3052040e539"} [mangiferin-p25989216] Mangiferin supplementation improves serum lipid profiles in overweight patients with hyperlipidemia: a double-blind randomized controlled trial. (2015). https://pubmed.ncbi.nlm.nih.gov/25989216/ DOI: 10.1038/srep10344
Complete structured claim and evidence
Mangiferin did not attenuate etoposide cytotoxicity in HL-60 cells, despite protecting cord-blood mononuclear cells in the comparison.
Mangiferin → Etoposide-associated cytotoxicity in human HL-60 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/24374812.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85ad69fcef2b1dd7b3842c076b89b76c9d54b73cc5843cefb3077642b6cb3451", "start_char": 0, "end_char": 1789, "text_sha256": "85ad69fcef2b1dd7b3842c076b89b76c9d54b73cc5843cefb3077642b6cb3451"}
experimental_model
Cell-line and primary mononuclear-cell comparison
exposure
Mangiferin 50 micromolar in principal assays; etoposide co-exposure
limitations
No clinical chemotherapy outcome. The abstract has an inconsistent mol/L unit in a later sentence; the 50 micromolar experimental concentration is explicit earlier.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
Protection varied with cell type.
primary_references
[mangiferin-p24374812] Mangiferin activates Nrf2-antioxidant response element signaling without reducing the sensitivity to etoposide of human myeloid leukemia cells in vitro. (2014). https://pubmed.ncbi.nlm.nih.gov/24374812/ DOI: 10.1038/aps.2013.165
tissue_or_cell_type
HL-60 leukemia cells and cord-blood mononuclear cells
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1303–1314
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-line and primary mononuclear-cell comparison · source_derived_draft · unverified_draft
### mangiferin-etoposide-cell-context Mangiferin did not attenuate etoposide cytotoxicity in HL-60 cells, despite protecting cord-blood mononuclear cells in the comparison. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection varied with cell type. organism: Homo sapiens tissue_or_cell_type: HL-60 leukemia cells and cord-blood mononuclear cells experimental_model: Cell-line and primary mononuclear-cell comparison limitations: No clinical chemotherapy outcome. The abstract has an inconsistent mol/L unit in a later sentence; the 50 micromolar experimental concentration is explicit earlier. exposure: Mangiferin 50 micromolar in principal assays; etoposide co-exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/24374812.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85ad69fcef2b1dd7b3842c076b89b76c9d54b73cc5843cefb3077642b6cb3451", "start_char": 0, "end_char": 1789, "text_sha256": "85ad69fcef2b1dd7b3842c076b89b76c9d54b73cc5843cefb3077642b6cb3451"} [mangiferin-p24374812] Mangiferin activates Nrf2-antioxidant response element signaling without reducing the sensitivity to etoposide of human myeloid leukemia cells in vitro. (2014). https://pubmed.ncbi.nlm.nih.gov/24374812/ DOI: 10.1038/aps.2013.165
Complete structured claim and evidence
Mangiferin increased PPAR-gamma expression in the chondrocyte experiment.
Mangiferin → Human PPAR gamma / PPARG source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"}
experimental_model
IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation
exposure
Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662
limitations
Cell experiment, not a clinical arthritis trial; inhibitor reversal supports involvement but not direct receptor agonism.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A transcriptional regulator participated in the response.
primary_references
[mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
tissue_or_cell_type
Cultured chondrocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1316–1327
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation · source_derived_draft · unverified_draft
### mangiferin-pparg Mangiferin increased PPAR-gamma expression in the chondrocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transcriptional regulator participated in the response. organism: Homo sapiens tissue_or_cell_type: Cultured chondrocytes experimental_model: IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation limitations: Cell experiment, not a clinical arthritis trial; inhibitor reversal supports involvement but not direct receptor agonism. exposure: Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662 evidence_span: {"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"} [mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
Complete structured claim and evidence
Mangiferin inhibited IL-1beta-associated NF-kappa-B activation.
Mangiferin → NF-kappa-B activation in human osteoarthritis chondrocytes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"}
experimental_model
IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation
exposure
Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662
limitations
Cell experiment, not a clinical arthritis trial; inhibitor reversal supports involvement but not direct receptor agonism.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
An inflammatory signaling readout was reduced.
primary_references
[mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
tissue_or_cell_type
Cultured chondrocytes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1329–1340
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation · source_derived_draft · unverified_draft
### mangiferin-nfkb Mangiferin inhibited IL-1beta-associated NF-kappa-B activation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory signaling readout was reduced. organism: Homo sapiens tissue_or_cell_type: Cultured chondrocytes experimental_model: IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation limitations: Cell experiment, not a clinical arthritis trial; inhibitor reversal supports involvement but not direct receptor agonism. exposure: Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662 evidence_span: {"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"} [mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
Complete structured claim and evidence
GW9662 reversed the anti-inflammatory effect of mangiferin in the chondrocyte study.
GW9662 → Inflammatory response in human osteoarthritis chondrocytes source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"}
experimental_model
IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation
exposure
Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662
limitations
The indexed abstract reports reversal of anti-inflammatory effects collectively; endpoint-specific magnitude is unresolved.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
Blocking related machinery weakened the response.
primary_references
[mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
tissue_or_cell_type
Cultured chondrocytes
trigger_kind
machinery_impairment Imported condition classification; unverified.
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1342–1353
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation · source_derived_draft · unverified_draft
### mangiferin-pparg-loss GW9662 reversed the anti-inflammatory effect of mangiferin in the chondrocyte study. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking related machinery weakened the response. organism: Homo sapiens tissue_or_cell_type: Cultured chondrocytes experimental_model: IL-1beta-stimulated osteoarthritis chondrocytes with inhibitor perturbation limitations: The indexed abstract reports reversal of anti-inflammatory effects collectively; endpoint-specific magnitude is unresolved. exposure: Mangiferin with IL-1beta; PPAR-gamma inhibitor GW9662 evidence_span: {"source_cache": "artifacts/mangiferin-research/27734234.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44", "start_char": 0, "end_char": 1007, "text_sha256": "1b9924d15171028fb1006c5e72c7b0dc6742d96f6873a292e6f5741061ad2f44"} [mangiferin-p27734234] Mangiferin Inhibits IL-1β-Induced Inflammatory Response by Activating PPAR-γ in Human Osteoarthritis Chondrocytes. (2017). https://pubmed.ncbi.nlm.nih.gov/27734234/ DOI: 10.1007/s10753-016-0451-y
Complete structured claim and evidence
Combinations of mangiferin with tested anticancer drugs reduced myeloma-cell viability more than the agents separately.
Mangiferin → Anticancer-drug cytotoxicity in human myeloma-cell combinations source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/27035859.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e", "start_char": 0, "end_char": 1327, "text_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e"}
experimental_model
Anticancer drug-combination experiments in myeloma cell lines
exposure
Mangiferin plus conventional anticancer agents; individual regimen not assigned from abstract
limitations
Cell viability and apoptosis findings do not establish clinical combination safety, benefit or formal pharmacologic synergy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
A combination effect was observed in cell culture.
primary_references
[mangiferin-p27035859] Mangiferin enhances the sensitivity of human multiple myeloma cells to anticancer drugs through suppression of the nuclear factor κB pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27035859/ DOI: 10.3892/ijo.2016.3470
tissue_or_cell_type
Multiple-myeloma cell lines
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1355–1366
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anticancer drug-combination experiments in myeloma cell lines · source_derived_draft · unverified_draft
### mangiferin-myeloma-combination Combinations of mangiferin with tested anticancer drugs reduced myeloma-cell viability more than the agents separately. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combination effect was observed in cell culture. organism: Homo sapiens tissue_or_cell_type: Multiple-myeloma cell lines experimental_model: Anticancer drug-combination experiments in myeloma cell lines limitations: Cell viability and apoptosis findings do not establish clinical combination safety, benefit or formal pharmacologic synergy. exposure: Mangiferin plus conventional anticancer agents; individual regimen not assigned from abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/27035859.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e", "start_char": 0, "end_char": 1327, "text_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e"} [mangiferin-p27035859] Mangiferin enhances the sensitivity of human multiple myeloma cells to anticancer drugs through suppression of the nuclear factor κB pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27035859/ DOI: 10.3892/ijo.2016.3470
Complete structured claim and evidence
The combination treatments increased caspase-3 activation in the myeloma-cell experiments.
Mangiferin → Caspase-3 activation in human myeloma-cell combinations source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mangiferin-research/27035859.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e", "start_char": 0, "end_char": 1327, "text_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e"}
experimental_model
Anticancer drug-combination experiments in myeloma cell lines
exposure
Mangiferin plus conventional anticancer agents; individual regimen not assigned from abstract
limitations
Cell viability and apoptosis findings do not establish clinical combination safety, benefit or formal pharmacologic synergy.
nutrient_topic
Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
organism
Homo sapiens
plain_language
Apoptosis machinery accompanied the viability response.
primary_references
[mangiferin-p27035859] Mangiferin enhances the sensitivity of human multiple myeloma cells to anticancer drugs through suppression of the nuclear factor κB pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27035859/ DOI: 10.3892/ijo.2016.3470
tissue_or_cell_type
Multiple-myeloma cell lines
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1368–1379
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anticancer drug-combination experiments in myeloma cell lines · source_derived_draft · unverified_draft
### mangiferin-myeloma-caspase The combination treatments increased caspase-3 activation in the myeloma-cell experiments. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Apoptosis machinery accompanied the viability response. organism: Homo sapiens tissue_or_cell_type: Multiple-myeloma cell lines experimental_model: Anticancer drug-combination experiments in myeloma cell lines limitations: Cell viability and apoptosis findings do not establish clinical combination safety, benefit or formal pharmacologic synergy. exposure: Mangiferin plus conventional anticancer agents; individual regimen not assigned from abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/27035859.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e", "start_char": 0, "end_char": 1327, "text_sha256": "018c08f93a5101b1a7fbafdbc99357f6d4baa9eed19711ff63e6c7cd3d3ec13e"} [mangiferin-p27035859] Mangiferin enhances the sensitivity of human multiple myeloma cells to anticancer drugs through suppression of the nuclear factor κB pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27035859/ DOI: 10.3892/ijo.2016.3470
Complete structured claim and evidence
Human PDH E1 forms a covalent lactyl-ThDP intermediate from pyruvate and decarboxylates it, retaining the two-carbon fragment on ThDP.
Human pyruvate dehydrogenase E1 → Pyruvate source_derived_draftungraded
Experimental context and source evidence
evidence
[{"paper_key": "seifert-2006-pdh-catalysis", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Recombinant human E1; transient kinetics.
limitations
Purified-system evidence; nutritional response was not tested.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
Activated vitamin B1 temporarily holds pyruvate while one carbon leaves as carbon dioxide. This is the first reaction, before acetyl-CoA is made.
primary_references
[seifert-2006-pdh-catalysis] Direct kinetic evidence for half-of-the-sites reactivity in the E1 component of the human pyruvate dehydrogenase multienzyme complex through alternating sites cofactor activation (2006). https://pubmed.ncbi.nlm.nih.gov/17042496/ DOI: 10.1021/bi061582l
tissue_or_cell_type
Purified mitochondrial enzyme
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 663–674
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human E1; transient kinetics. · source_derived_draft · unverified_draft
### b1-pdh-pyruvate-covalent-decarboxylation Human PDH E1 forms a covalent lactyl-ThDP intermediate from pyruvate and decarboxylates it, retaining the two-carbon fragment on ThDP. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated vitamin B1 temporarily holds pyruvate while one carbon leaves as carbon dioxide. This is the first reaction, before acetyl-CoA is made. organism: Homo sapiens tissue_or_cell_type: Purified mitochondrial enzyme experimental_model: Recombinant human E1; transient kinetics. limitations: Purified-system evidence; nutritional response was not tested. evidence: [{"paper_key": "seifert-2006-pdh-catalysis", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] nutrient: Thiamine (vitamin B1) [seifert-2006-pdh-catalysis] Direct kinetic evidence for half-of-the-sites reactivity in the E1 component of the human pyruvate dehydrogenase multienzyme complex through alternating sites cofactor activation (2006). https://pubmed.ncbi.nlm.nih.gov/17042496/ DOI: 10.1021/bi061582l
Complete structured claim and evidence
The human DLAT catalytic core contains a channel for the acetylated lipoyl group and CoA; substrate modeling positions CoA for acetyl-CoA formation.
Dihydrolipoyl acetyltransferase / DLAT → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B1-dependent E1 and B5-derived CoA participate in different sequential steps.
evidence
[{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Human DLAT cryo-EM; bacterial ligand poses used for modeling.
limitations
Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier.
primary_references
[jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357
tissue_or_cell_type
Purified catalytic core
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 690–702
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DLAT cryo-EM; bacterial ligand poses used for modeling. · source_derived_draft · unverified_draft
### b1-pdh-dlat-coa-acetylation The human DLAT catalytic core contains a channel for the acetylated lipoyl group and CoA; substrate modeling positions CoA for acetyl-CoA formation. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier. organism: Homo sapiens tissue_or_cell_type: Purified catalytic core experimental_model: Human DLAT cryo-EM; bacterial ligand poses used for modeling. limitations: Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment. evidence: [{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1-dependent E1 and B5-derived CoA participate in different sequential steps. nutrient: Thiamine (vitamin B1) [jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357
Complete structured claim and evidence
Human DLD uses bound FAD and transiently bound NAD+ to oxidize dihydrolipoamide; NADH-bound structures place its nicotinamide ring beside FAD.
DLD → Protein-bound reduced dihydrolipoyl-lysine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B1 performs E1 carbon chemistry; B2-derived FAD and the niacin-related NAD cofactor participate in the separate shared E3 reaction.
evidence
[{"paper_key": "brautigam-2005-dld", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Human DLD crystallography with NAD+ and NADH.
limitations
Cofactor chemistry does not establish dietary B2/B3 limitation or prove rescue of B1 deficiency.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
The shared E3 protein resets reduced lipoyl carriers using the B2-derived flavin and B3-related NAD system, allowing another round of B1-dependent turnover.
primary_references
[brautigam-2005-dld] Crystal structure of human dihydrolipoamide dehydrogenase: NAD+/NADH binding and the structural basis of disease-causing mutations (2005). https://pubmed.ncbi.nlm.nih.gov/15946682/ DOI: 10.1016/j.jmb.2005.05.014
tissue_or_cell_type
Purified enzyme
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 717–729
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DLD crystallography with NAD+ and NADH. · source_derived_draft · unverified_draft
### b1-dld-fad-nad-lipoyl-regeneration Human DLD uses bound FAD and transiently bound NAD+ to oxidize dihydrolipoamide; NADH-bound structures place its nicotinamide ring beside FAD. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The shared E3 protein resets reduced lipoyl carriers using the B2-derived flavin and B3-related NAD system, allowing another round of B1-dependent turnover. organism: Homo sapiens tissue_or_cell_type: Purified enzyme experimental_model: Human DLD crystallography with NAD+ and NADH. limitations: Cofactor chemistry does not establish dietary B2/B3 limitation or prove rescue of B1 deficiency. evidence: [{"paper_key": "brautigam-2005-dld", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1 performs E1 carbon chemistry; B2-derived FAD and the niacin-related NAD cofactor participate in the separate shared E3 reaction. nutrient: Thiamine (vitamin B1) [brautigam-2005-dld] Crystal structure of human dihydrolipoamide dehydrogenase: NAD+/NADH binding and the structural basis of disease-causing mutations (2005). https://pubmed.ncbi.nlm.nih.gov/15946682/ DOI: 10.1016/j.jmb.2005.05.014
Complete structured claim and evidence
Human SIRT1 removes acetylation from histone H4 Lys16 in an NAD+-dependent reaction.
SIRT1 → Histone H4 acetylated at K16 source_derived_draftungraded
Experimental context and source evidence
experimental_model
Human enzyme assays and cultured-cell SIRT1 perturbation.
limitations
This reaction modifies lysine already in a protein. It does not show that extra oral lysine increases the reaction or improves a clinical outcome.
organism
Human
plain_language
A different enzyme removes a lysine modification using NAD+.
primary_references
[sirt1-2004] Human SirT1 interacts with histone H1 and promotes formation of facultative heterochromatin (2004). https://pubmed.ncbi.nlm.nih.gov/15469825/ DOI: 10.1016/j.molcel.2004.08.031
tissue_or_cell_type
Not specified as a whole tissue; see experimental model.
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 537–545
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme assays and cultured-cell SIRT1 perturbation. · source_derived_draft · unverified_draft
### sirt1-h4k16-deacetylation Human SIRT1 removes acetylation from histone H4 Lys16 in an NAD+-dependent reaction. Plain language: A different enzyme removes a lysine modification using NAD+. Condition category: normal organism: Human tissue_or_cell_type: Not specified as a whole tissue; see experimental model. experimental_model: Human enzyme assays and cultured-cell SIRT1 perturbation. limitations: This reaction modifies lysine already in a protein. It does not show that extra oral lysine increases the reaction or improves a clinical outcome. [sirt1-2004] Human SirT1 interacts with histone H1 and promotes formation of facultative heterochromatin (2004). https://pubmed.ncbi.nlm.nih.gov/15469825/ DOI: 10.1016/j.molcel.2004.08.031
Complete structured claim and evidence
The human SOD2 active-site manganese is coordinated by His26, His74, His163, Asp159 and a water/hydroxide ligand in the structural model.
Mn2+ → Human mitochondrial manganese superoxide dismutase / SOD2 source_derived_draftungraded
Experimental context and source evidence
experimental_model
Redox-controlled neutron structures of human SOD2
exposure
Redox-controlled Mn(III) and Mn(II) crystals
limitations
Primary experimental scope only; no human dietary threshold, clinical treatment rule, or universal metal substitution is established.
nutrient_topic
Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
organism
Homo sapiens
plain_language
A defined protein pocket holds manganese for SOD2 chemistry.
primary_references
[mn-enz-33824320] Direct detection of coupled proton and electron transfers in human manganese superoxide dismutase. (2021). https://pubmed.ncbi.nlm.nih.gov/33824320/ DOI: 10.1038/s41467-021-22290-1
tissue_or_cell_type
Purified enzyme; mitochondrial-matrix protein
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 434–444
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Redox-controlled neutron structures of human SOD2 · source_derived_draft · unverified_draft
### mn-enz-sod2-coordination The human SOD2 active-site manganese is coordinated by His26, His74, His163, Asp159 and a water/hydroxide ligand in the structural model. Condition category: normal nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defined protein pocket holds manganese for SOD2 chemistry. organism: Homo sapiens tissue_or_cell_type: Purified enzyme; mitochondrial-matrix protein experimental_model: Redox-controlled neutron structures of human SOD2 limitations: Primary experimental scope only; no human dietary threshold, clinical treatment rule, or universal metal substitution is established. exposure: Redox-controlled Mn(III) and Mn(II) crystals [mn-enz-33824320] Direct detection of coupled proton and electron transfers in human manganese superoxide dismutase. (2021). https://pubmed.ncbi.nlm.nih.gov/33824320/ DOI: 10.1038/s41467-021-22290-1
Complete structured claim and evidence
Human OCTN2 expression increased sodium-dependent carnitine uptake with an apparent Km of 4.34 micromolar.
Human carnitine transporter OCTN2 / SLC22A5 → L-Carnitine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/9685390.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6", "start_char": 0, "end_char": 1549, "text_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6"}
experimental_model
Cloning and functional expression
exposure
Radiolabeled carnitine uptake and sodium dependence
limitations
Expression assay; dietary sodium intake, mitochondrial fatty-acid oxidation and clinical supplementation were not directly tested.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human OCTN2 in HEK293 cells
plain_language
The sodium gradient helps bring carnitine into cells.
primary_references
[sodium-p9685390] Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. (1998). https://pubmed.ncbi.nlm.nih.gov/9685390/ DOI: 10.1074/jbc.273.32.20378
tissue_or_cell_type
Cell plasma membrane
transport_effect
raises Expression increased sodium-dependent carnitine uptake.
transport_pool
the expressing cell Expression increased sodium-dependent carnitine uptake.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 616–627
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and functional expression · source_derived_draft · unverified_draft
### sodium-octn2-carnitine Human OCTN2 expression increased sodium-dependent carnitine uptake with an apparent Km of 4.34 micromolar. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium gradient helps bring carnitine into cells. organism: Human OCTN2 in HEK293 cells tissue_or_cell_type: Cell plasma membrane experimental_model: Cloning and functional expression limitations: Expression assay; dietary sodium intake, mitochondrial fatty-acid oxidation and clinical supplementation were not directly tested. exposure: Radiolabeled carnitine uptake and sodium dependence evidence_span: {"source_cache": "artifacts/sodium-research/9685390.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6", "start_char": 0, "end_char": 1549, "text_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6"} [sodium-p9685390] Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. (1998). https://pubmed.ncbi.nlm.nih.gov/9685390/ DOI: 10.1074/jbc.273.32.20378
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

When bacterial gene expression is inhibited

Condition: machinery_impairment · Rifampicin or chloramphenicol in the bacterial experiment.

Normal role: Induced bacterial machinery can convert mangiferin to norathyriol.

Recorded consequence: C-glucosyl cleavage was abolished.

Scope: Bacteroides sp. MANG culture

When LKB1 is experimentally depleted

Condition: machinery_impairment · LKB1 siRNA knockdown in sodium-oleate-loaded HepG2 cells.

Normal role: LKB1 participates upstream of AMPK in this cellular response.

Recorded consequence: Norathyriol failed to lower triglycerides or increase AMPK/ACC phosphorylation.

Scope: Human HepG2 cells

When HO-1 activity is inhibited

Condition: machinery_impairment · Pharmacological HO-1 inhibition during mangiferin/H2O2 treatment.

Normal role: HO-1 contributes to the protective response in this assay.

Recorded consequence: ROS suppression and cytoprotective effects were attenuated.

Scope: Human ARPE-19 cells

When PPAR-gamma signaling is inhibited

Condition: machinery_impairment · GW9662 during the mangiferin/IL-1beta experiment.

Normal role: PPAR-gamma contributes to the response in this cell experiment.

Recorded consequence: Anti-inflammatory effects were reversed.

Scope: Human osteoarthritis chondrocytes

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

L-Lysine: mechanism-first literature curation (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

How much norathyriol reaches human tissues after each mangiferin formulation?Human parent-compound pharmacokinetics and ex vivo conversion do not quantify tissue exposure to the aglycone and conjugates.
Does changing pectin intake modify oral mangiferin exposure?An engineered encapsulation matrix is not a dietary co-ingestion experiment.
Do the lipid-trial findings replicate and improve patient-important outcomes?The selected randomized trial measured 12-week biomarkers; it does not establish cardiovascular event reduction, long-term safety or general benefit.
Which features explain renal transporter downregulation in the earlier rodent models but not in the nephropathy model?Both published observations are retained. Model, regimen and tissue injury differ; these studies do not resolve the responsible variable or establish a same-condition contradiction.
Do mangiferin or norathyriol alter drug exposure at achievable human doses?Human hepatocyte and recombinant-enzyme findings identify candidates, not validated clinical drug interactions.
Does oral mangiferin change human iron absorption, iron status or the response to iron supplements?The selected metal-complexing experiments do not measure human iron balance.
Can mangiferin improve PDH flux when thiamine, riboflavin, niacin, CoA or protein lipoylation is limiting?The selected activation study did not test these deficiencies; a shared enzyme does not establish rescue or supplementation synergy.
Does SIRT1 involvement make mangiferin and niacin supplementation synergistic?NAD dependence is established background, but this combination was not tested in the selected mechanism study.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Mangiferin

The mechanisms

An inducible activity in Bacteroides sp. MANG cleaved mangiferin to norathyriol.

After 0.9 g orally, plasma mangiferin peaked at 38.64 +/- 6.75 ng/mL at about one hour; apparent half-life was 7.85 +/- 1.72 hours.

Mangiferin prevented ascorbate-driven ferric iron reduction in vitro.

Mangiferin exposure increased susceptibility to calcium-induced mitochondrial permeability transition.

The ferric complex did not elicit permeability transition and protected against its induction in the assay.

PDH activity increased in assays using mitochondrial protein from mangiferin-treated C2C12 cells.

LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation.

Mangiferin opposed H2O2-associated loss of manganese superoxide dismutase expression and activity.

Norathyriol competitively inhibited UGT1A9; IC50 12.3 and Ki 2.8 micromolar.

Serum triglycerides were lower with mangiferin than placebo.

Serum L-carnitine increased compared with placebo.

Serum glucose did not differ significantly between groups.

The rifampicin treatment abolished the induced C-glucosyl-cleaving activity.

The chloramphenicol treatment abolished the induced C-glucosyl-cleaving activity.

Fecal cultures converted mangiferin to norathyriol with donor-dependent variation.

Norathyriol reduced overall bacterial cell counts in the tested cultures.

Norathyriol suppressed Faecalibacterium prausnitzii in the culture comparison.

Norathyriol suppressed the urate-consuming species Enterocloster bolteae in culture.

Norathyriol absolute bioavailability was 30.4% in the rat experiment.

Norathyriol glucuronides were prominent circulating conjugates after administration in rats.

Norathyriol sulfates were prominent circulating conjugates after administration in rats.

Human mangiferin pharmacokinetics were nonlinear across the tested doses.

MLES produced 2.44-fold higher AUC over 24 hours than MLE60 in the crossover comparison.

The spray-dried cashew-pectin system encapsulated mangiferin with reported efficiency of 82.02%.

Mangiferin increased glucose oxidation in the studied mouse-muscle systems.

Mangiferin increased pyruvate oxidation in C2C12 myotubes.

Mangiferin reduced anaerobic pyruvate-to-lactate metabolism in the cell experiments.

Mangiferin did not increase fatty acid oxidation in these muscle-cell experiments.

After 24 hours, mangiferin reduced PDK4 protein abundance in C2C12 cells.

After 15 minutes, PDH phosphorylation decreased without a detected change in PDK4 abundance.

Mangiferin increased AMPK phosphorylation in L6 myotubes.

Norathyriol increased AMPK phosphorylation in L6 myotubes.

Mangiferin did not increase Akt phosphorylation in the reported assay.

In insulin-resistant L6 cells, mangiferin increased glucose consumption only with insulin co-treatment; norathyriol worked with or without insulin.

Mangiferin and tested metabolites were not direct AMPK activators in the HTRF assay.

Norathyriol increased SIRT1 protein expression in HepG2 cells.

Norathyriol lowered measured LKB1 acetylation in HepG2 cells.

Norathyriol increased the cellular AMP-to-ATP ratio in the tested HepG2 model.

LKB1 knockdown blocked the triglyceride-lowering response to norathyriol.

LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation.

Nrf2 half-life increased from 20 to 58 minutes in the HL-60 chase experiment.

Immunoprecipitation showed reduced Nrf2 ubiquitination after mangiferin treatment.

Mangiferin did not change the Nrf2 mRNA level in this study.

Mangiferin increased nuclear Nrf2 accumulation.

Mangiferin increased NQO1 expression in cord-blood mononuclear cells.

Mangiferin reduced etoposide-associated comet and micronucleus damage readouts.

Mangiferin preserved the glutathione pool during H2O2 exposure.

Mangiferin opposed H2O2-associated loss of glutathione peroxidase expression and activity.

Mangiferin increased HO-1 expression and activity in ARPE-19 cells.

HO-1 inhibition attenuated the protective effect of mangiferin against H2O2 injury.

Mangiferin inhibited ferrous-citrate-triggered mitochondrial lipid peroxidation.

Mangiferin accelerated ferrous iron autoxidation in the tested system.

Calcium-challenged mitochondria from treated rats showed glutathione depletion.

Electrochemical and spectroscopic analyses supported coordination of ferric iron with mangiferin.

The ferric complex protected mitochondrial glutathione against oxidation.

Mangiferin reduced measured CYP1A2 activity in the hepatocyte experiment.

Mangiferin reduced measured CYP2A6 activity in the hepatocyte experiment.

Mangiferin reduced measured CYP2C9 activity in the hepatocyte experiment.

Mangiferin reduced measured CYP2D6 activity in the hepatocyte experiment.

Mangiferin reduced measured CYP3A4 activity in the hepatocyte experiment.

At 250 micrograms/mL, mangiferin reduced UGT1A1 activity by about 55 percent.

At 250 micrograms/mL, mangiferin reduced UGT2B7 activity by about 55 percent.

At 250 micrograms/mL, mangiferin reduced UGT1A9 activity by about 35 percent.

Norathyriol competitively inhibited UGT1A3; IC50 8.2 and Ki 1.6 micromolar.

Norathyriol competitively inhibited UGT1A7; IC50 4.4 and Ki 2.0 micromolar.

Mangiferin reduced renal Rat urate transporter 1 / Slc22a12 mRNA and protein in hyperuricemic rats.

Mangiferin reduced renal Rat organic anion transporter 10 / Slc22a13 mRNA and protein in hyperuricemic rats.

Mangiferin reduced renal Rat glucose transporter 9 / Slc2a9 mRNA and protein in hyperuricemic rats.

Renal PDZK1 expression was not altered in the same rat experiment.

Mangiferin reduced renal Mouse urate transporter 1 / Slc22a12 expression in the hyperuricemic mice.

Mangiferin reduced renal Mouse glucose transporter 9 / Slc2a9 expression in the hyperuricemic mice.

Mangiferin increased renal Mouse organic anion transporter 1 / Slc22a6 expression in the hyperuricemic mice.

Mangiferin increased renal Mouse carnitine transporter Octn2 / Slc22a5 expression in the hyperuricemic mice.

Mangiferin reduced renal AQP2 protein expression in nephropathy mice.

Urine volume increased without a marked change in urine urate concentration.

No change in renal Mouse urate transporter 1 / Slc22a12 expression was detected in the nephropathy model.

No change in renal Mouse glucose transporter 9 / Slc2a9 expression was detected in the nephropathy model.

No change in renal Mouse organic anion transporter 1 / Slc22a6 expression was detected in the nephropathy model.