Mouse Nrf2 / Nfe2l2

evidence_span

{"source_cache": "artifacts/chlorogenic_acid-research/41862684.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644", "start_char": 0, "end_char": 1292, "text_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644"}

experimental_model

Mouse hepatectomy, genetic tests and Keap1-binding investigation

exposure

CGA treatment; doses not provided in indexed abstract

limitations

Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Mus musculus; binding preparation species not resolved from abstract

plain_language

The response connects to machinery controlling cell division.

primary_references

[chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

tissue_or_cell_type

Regenerating liver after 70% or 90% partial hepatectomy

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 555–566

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hepatectomy, genetic tests and Keap1-binding investigation · source_derived_draft · unverified_draft

### chlorogenic_acid-nrf2-e2f1 Nrf2 activation increased E2F1 mRNA in the regeneration model. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response connects to machinery controlling cell division. organism: Mus musculus; binding preparation species not resolved from abstract tissue_or_cell_type: Regenerating liver after 70% or 90% partial hepatectomy experimental_model: Mouse hepatectomy, genetic tests and Keap1-binding investigation limitations: Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred. exposure: CGA treatment; doses not provided in indexed abstract evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/41862684.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644", "start_char": 0, "end_char": 1292, "text_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644"} [chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

evidence_span

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experimental_model

Mouse hepatectomy, genetic tests and Keap1-binding investigation

exposure

CGA treatment; doses not provided in indexed abstract

limitations

Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Mus musculus; binding preparation species not resolved from abstract

plain_language

A second branch connects the response to energy metabolism.

primary_references

[chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

tissue_or_cell_type

Regenerating liver after 70% or 90% partial hepatectomy

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 581–592

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hepatectomy, genetic tests and Keap1-binding investigation · source_derived_draft · unverified_draft

### chlorogenic_acid-nrf2-pgc1 Nrf2 activation increased PGC-1alpha mRNA in the regeneration model. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second branch connects the response to energy metabolism. organism: Mus musculus; binding preparation species not resolved from abstract tissue_or_cell_type: Regenerating liver after 70% or 90% partial hepatectomy experimental_model: Mouse hepatectomy, genetic tests and Keap1-binding investigation limitations: Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred. exposure: CGA treatment; doses not provided in indexed abstract evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/41862684.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644", "start_char": 0, "end_char": 1292, "text_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644"} [chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Wild-type versus Nrf2-null mice.

limitations

Knockout context does not define a dietary deficiency.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

Removing the regulator changed the response to the compound.

primary_references

Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24747074/ · DOI 10.1016/j.bbrc.2014.04.039

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 460–466

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Wild-type versus Nrf2-null mice. · source_derived_draft · unverified_draft

## luteolin-mouse-nrf2-loss Removing the regulator changed the response to the compound. The distinct luteolin-associated liver responses were absent in Nrf2-knockout mice. Model: Wild-type versus Nrf2-null mice. Limitations: Knockout context does not define a dietary deficiency. Evidence access: Primary abstract Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24747074/ · DOI 10.1016/j.bbrc.2014.04.039

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Mouse microglial cells; Nrf2 knockdown and metal comparisons.

limitations

Endpoint-specific response; not total suppression of immunity.

nutrient_topic

Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

plain_language

Even inflammatory outputs had different dependencies.

primary_references

Modulation of the Neuroprotective and Anti-inflammatory Activities of the Flavonol Fisetin by the Transition Metals Iron and Copper. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33187316/ · DOI 10.3390/antiox9111113

trigger_kind

machinery_impairment Imported condition classification; unverified.

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 176–182

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse microglial cells; Nrf2 knockdown and metal comparisons. · source_derived_draft · unverified_draft

## fisetin-microglial-nrf2-dependence Even inflammatory outputs had different dependencies. Nrf2 siRNA weakened fisetin suppression of nitric oxide and IL-6, but not TNF-alpha to the same extent, in LPS-treated mouse BV2 cells. Model: Mouse microglial cells; Nrf2 knockdown and metal comparisons. Limitations: Endpoint-specific response; not total suppression of immunity. Evidence access: Primary full text Modulation of the Neuroprotective and Anti-inflammatory Activities of the Flavonol Fisetin by the Transition Metals Iron and Copper. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33187316/ · DOI 10.3390/antiox9111113

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Mouse-cell gene-silencing comparisons.

limitations

Cooperation in this assay is not proof of universal transcriptional synergy.

nutrient_topic

Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

plain_language

The cell relies on both regulators during stress.

primary_references

Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

trigger_kind

machinery_impairment Imported condition classification; unverified.

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 128–134

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-cell gene-silencing comparisons. · source_derived_draft · unverified_draft

## fisetin-stress-cooperation The cell relies on both regulators during stress. Under oxidative stress, siRNA experiments implicated both Nrf2 and ATF4 in the mouse-cell glutathione response to fisetin. Model: Mouse-cell gene-silencing comparisons. Limitations: Cooperation in this assay is not proof of universal transcriptional synergy. Evidence access: Primary abstract Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

acting_entity

mouse-nfe2l2

availability_state

machinery_impairment Imported condition classification; unverified.

dose

Not specified in accessed abstract

duration

Not specified in accessed abstract

evidence_access

Primary abstract

experimental_comparison

SAC versus ischemic control; wild-type versus Nrf2 knockout

experimental_model

Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice

interpretation_status

Source-derived research curation; not independent primary verification

limitations

Necessity in this model; not proof that every SAC effect requires Nrf2.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Mus musculus

plain_language

Removing the pathway changed the response to SAC.

primary_references

[25393425] S-allyl cysteine activates the Nrf2-dependent antioxidant response and protects neurons against ischemic injury in vitro and in vivo. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25393425/ · DOI 10.1111/jnc.12986

route

Systemic administration; precise route not retrieved

tissue_or_cell_type

Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice

trigger_kind

machinery_impairment Imported condition classification; unverified.

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 140–147

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice · source_derived_draft · unverified_draft

## s-allylcysteine-mouse-nrf2-required Removing the pathway changed the response to SAC. Nrf2 knockout mice did not show the ischemic protection observed with systemic SAC in wild-type mice. Model: Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice Limitations: Necessity in this model; not proof that every SAC effect requires Nrf2. Evidence access: Primary abstract [25393425] S-allyl cysteine activates the Nrf2-dependent antioxidant response and protects neurons against ischemic injury in vitro and in vivo. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25393425/ · DOI 10.1111/jnc.12986 Structured context: {"organism": "Mus musculus", "tissue_or_cell_type": "Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice", "dose": "Not specified in accessed abstract", "duration": "Not specified in accessed abstract", "route": "Systemic administration; precise route not retrieved", "experimental_comparison": "SAC versus ischemic control; wild-type versus Nrf2 knockout", "acting_entity": "mouse-nfe2l2", "interpretation_status": "Source-derived research curation; not independent primary verification"}

evidence_span

{"source_cache": "artifacts/chlorogenic_acid-research/41862684.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644", "start_char": 0, "end_char": 1292, "text_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644"}

experimental_model

Mouse hepatectomy, genetic tests and Keap1-binding investigation

exposure

CGA treatment; doses not provided in indexed abstract

limitations

Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Mus musculus; binding preparation species not resolved from abstract

plain_language

Releasing a transcriptional response was associated with regeneration.

primary_references

[chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

tissue_or_cell_type

Regenerating liver after 70% or 90% partial hepatectomy

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 542–553

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hepatectomy, genetic tests and Keap1-binding investigation · source_derived_draft · unverified_draft

### chlorogenic_acid-mouse-nrf2 The mouse regeneration study linked CGA-Keap1 interaction to Nrf2 activation. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Releasing a transcriptional response was associated with regeneration. organism: Mus musculus; binding preparation species not resolved from abstract tissue_or_cell_type: Regenerating liver after 70% or 90% partial hepatectomy experimental_model: Mouse hepatectomy, genetic tests and Keap1-binding investigation limitations: Surgical mouse regeneration is not chronic human fatty-liver treatment. Arg415 binding was reported but the abstract does not identify the species of every recombinant construct; no human KEAP1 residue-specific edge is inferred. exposure: CGA treatment; doses not provided in indexed abstract evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/41862684.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644", "start_char": 0, "end_char": 1292, "text_sha256": "7246caa586cbd35b79fa9518b522dc7c1d330aad71c98611ae7cc763f7952644"} [chlorogenic_acid-p41862684] Chlorogenic acid promotes liver regeneration after partial hepatectomy through activating Nrf2 via directly targeting Keap1. (2026). https://pubmed.ncbi.nlm.nih.gov/41862684/ DOI: 10.1038/s41401-026-01770-4

evidence_span

{"source_cache": "artifacts/dim-research/21615272.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8", "start_char": 0, "end_char": 737, "text_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8"}

experimental_model

Reporter and gene/protein expression experiments

exposure

DIM compared with I3C and sulforaphane

limitations

Mouse cells; transcriptional induction does not establish clinical antioxidant benefit or nutrient repletion.

nutrient_topic

Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM

organism

Mouse NIH3T3 fibroblasts

plain_language

A chemical conversion changed signaling activity in this model.

primary_references

[dim-p21615272] 3,3'-Diindolylmethane but not indole-3-carbinol activates Nrf2 and induces Nrf2 target gene expression in cultured murine fibroblasts. (2011). https://pubmed.ncbi.nlm.nih.gov/21615272/ DOI: 10.3109/10715762.2011.571683

tissue_or_cell_type

Nrf2-regulated defense genes

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1234–1245

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reporter and gene/protein expression experiments · source_derived_draft · unverified_draft

### dim-mouse-nrf2 DIM activated Nrf2-dependent transcription in mouse fibroblasts, whereas I3C did not in the tested conditions. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemical conversion changed signaling activity in this model. organism: Mouse NIH3T3 fibroblasts tissue_or_cell_type: Nrf2-regulated defense genes experimental_model: Reporter and gene/protein expression experiments limitations: Mouse cells; transcriptional induction does not establish clinical antioxidant benefit or nutrient repletion. exposure: DIM compared with I3C and sulforaphane evidence_span: {"source_cache": "artifacts/dim-research/21615272.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8", "start_char": 0, "end_char": 737, "text_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8"} [dim-p21615272] 3,3'-Diindolylmethane but not indole-3-carbinol activates Nrf2 and induces Nrf2 target gene expression in cultured murine fibroblasts. (2011). https://pubmed.ncbi.nlm.nih.gov/21615272/ DOI: 10.3109/10715762.2011.571683

evidence_access

Primary full text

experimental_model

5 micromolar fisetin with FeCl2/CuCl2 titration.

limitations

Cell-culture ratio, not a clinical spacing rule for supplements.

nutrient_topic

Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

plain_language

Iron weakened the signaling response under these conditions.

primary_references

Modulation of the Neuroprotective and Anti-inflammatory Activities of the Flavonol Fisetin by the Transition Metals Iron and Copper. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33187316/ · DOI 10.3390/antiox9111113

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 160–166

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 5 micromolar fisetin with FeCl2/CuCl2 titration. · source_derived_draft · unverified_draft

## fisetin-iron-signaling-antagonism Iron weakened the signaling response under these conditions. In mouse HT22 cells, added iron reduced fisetin-induced nuclear Nrf2 and ATF4 from an iron:fisetin ratio of 0.5:1; copper did not do so in the tested range. Model: 5 micromolar fisetin with FeCl2/CuCl2 titration. Limitations: Cell-culture ratio, not a clinical spacing rule for supplements. Evidence access: Primary full text Modulation of the Neuroprotective and Anti-inflammatory Activities of the Flavonol Fisetin by the Transition Metals Iron and Copper. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33187316/ · DOI 10.3390/antiox9111113

evidence_access

Primary abstract

experimental_model

Primary abstract plus PubMed mouse-protein indexing.

limitations

No direct Nrf2 binding site or specific KEAP1 reaction established here.

nutrient_topic

Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

plain_language

Stress-defense transcription can stay active for longer.

primary_references

Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 104–110

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary abstract plus PubMed mouse-protein indexing. · source_derived_draft · unverified_draft

## fisetin-nrf2-stability Stress-defense transcription can stay active for longer. In the mouse-cell study, fisetin increased Nrf2 stability and Nrf2-dependent transcription. Model: Primary abstract plus PubMed mouse-protein indexing. Limitations: No direct Nrf2 binding site or specific KEAP1 reaction established here. Evidence access: Primary abstract Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Mouse embryonic fibroblasts and human DU-145 cells

plain_language

PERK was also needed for the measured movement of Nrf2 into the nucleus.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

Cell culture

trigger_kind

machinery_impairment Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 508–519

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-perk-nrf2-dependence Boric acid induced Nrf2 nuclear translocation in wild-type mouse fibroblasts but not in Perk-null cells. Condition category: machinery_impairment nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: PERK was also needed for the measured movement of Nrf2 into the nucleus. organism: Mouse embryonic fibroblasts and human DU-145 cells tissue_or_cell_type: Cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_access

Primary abstract

experimental_model

Mouse chemically induced fulminant hepatitis.

limitations

Not universal Nrf2 activation or evidence of clinical hepatoprotection. The abstract calls myricetin a glycoside; this collection retains its correct aglycone identity.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

A defense regulator increased in this liver-injury model.

primary_references

The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 636–642

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse chemically induced fulminant hepatitis. · source_derived_draft · unverified_draft

## myricetin-mouse-nrf2 A defense regulator increased in this liver-injury model. Myricetin increased hepatic Nrf2 expression in mice challenged with LPS/D-galactosamine. Model: Mouse chemically induced fulminant hepatitis. Limitations: Not universal Nrf2 activation or evidence of clinical hepatoprotection. The abstract calls myricetin a glycoside; this collection retains its correct aglycone identity. Evidence access: Primary abstract The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075

acting_entity

s-allylcysteine

dose

Not specified in accessed abstract

duration

Not specified in accessed abstract

evidence_access

Primary abstract

experimental_comparison

SAC versus ischemic control; wild-type versus Nrf2 knockout

experimental_model

Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice

interpretation_status

Source-derived research curation; not independent primary verification

limitations

No direct binding site or therapeutic human exposure is established by these experiments.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Mus musculus

plain_language

A cellular defense response changed after treatment.

primary_references

[25393425] S-allyl cysteine activates the Nrf2-dependent antioxidant response and protects neurons against ischemic injury in vitro and in vivo. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25393425/ · DOI 10.1111/jnc.12986

route

Systemic administration; precise route not retrieved

tissue_or_cell_type

Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 131–138

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice · source_derived_draft · unverified_draft

## s-allylcysteine-mouse-nrf2 A cellular defense response changed after treatment. SAC administration increased Nrf2 protein and antioxidant-response signaling in the mouse ischemia study. Model: Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice Limitations: No direct binding site or therapeutic human exposure is established by these experiments. Evidence access: Primary abstract [25393425] S-allyl cysteine activates the Nrf2-dependent antioxidant response and protects neurons against ischemic injury in vitro and in vivo. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25393425/ · DOI 10.1111/jnc.12986 Structured context: {"organism": "Mus musculus", "tissue_or_cell_type": "Middle cerebral artery occlusion in wild-type and Nrf2 knockout mice", "dose": "Not specified in accessed abstract", "duration": "Not specified in accessed abstract", "route": "Systemic administration; precise route not retrieved", "experimental_comparison": "SAC versus ischemic control; wild-type versus Nrf2 knockout", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}

dose

Cannabidiol 5 micromolar plus moringin 5 micromolar

duration

Acute

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

evidence_scope

literature_reviewed; model-specific source-derived curation

experimental_model

LPS-stimulated murine macrophages

limitations

This cell combination result does not establish clinical synergy, safety or dosing and should not be extrapolated to cannabis or whole Moringa products.

nutrient_topic

Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera

organism

LPS-stimulated murine macrophages

plain_language

Cannabidiol plus moringin, each at 5 micromolar, produced larger changes in inflammatory, oxidative and apoptosis markers in LPS-stimulated murine macrophages than either constituent alone at that concentration.

primary_references

Anti-inflammatory and antioxidant effects of a combination of cannabidiol and moringin in LPS-stimulated macrophages. (2016). https://pubmed.ncbi.nlm.nih.gov/27215129/ DOI: 10.1016/j.fitote.2016.05.008

route

In vitro

tissue

TNF-alpha, IL-10, iNOS, NRF2, nitrotyrosine, BCL2, BAX and cleaved-caspase-3 panel

Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 90–99

Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · LPS-stimulated murine macrophages · source_derived_draft · unverified_draft

## moringa-cannabidiol-combination Cannabidiol plus moringin, each at 5 micromolar, produced larger changes in inflammatory, oxidative and apoptosis markers in LPS-stimulated murine macrophages than either constituent alone at that concentration. Model/species: LPS-stimulated murine macrophages Tissue/system: TNF-alpha, IL-10, iNOS, NRF2, nitrotyrosine, BCL2, BAX and cleaved-caspase-3 panel Exposure: Cannabidiol 5 micromolar plus moringin 5 micromolar Route: In vitro Duration: Acute Limits: This cell combination result does not establish clinical synergy, safety or dosing and should not be extrapolated to cannabis or whole Moringa products. Primary reference: Anti-inflammatory and antioxidant effects of a combination of cannabidiol and moringin in LPS-stimulated macrophages. (2016). https://pubmed.ncbi.nlm.nih.gov/27215129/ DOI: 10.1016/j.fitote.2016.05.008 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

evidence_access

Primary full text

experimental_model

Mouse macrophage culture.

limitations

Expression alone does not show human glutathione restoration.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

A conjugate can influence glutathione-synthesis machinery.

primary_references

Anti-Inflammatory and Anti-Oxidative Effects of luteolin-7-O-glucuronide in LPS-Stimulated Murine Macrophages through TAK1 Inhibition and Nrf2 Activation. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32187984/ · DOI 10.3390/ijms21062007

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 508–514

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage culture. · source_derived_draft · unverified_draft

## luteolin-glucuronide-gclc A conjugate can influence glutathione-synthesis machinery. Luteolin 7-O-glucuronide increased GCLC expression alongside Nrf2 activation in RAW264.7 cells. Model: Mouse macrophage culture. Limitations: Expression alone does not show human glutathione restoration. Evidence access: Primary full text Anti-Inflammatory and Anti-Oxidative Effects of luteolin-7-O-glucuronide in LPS-Stimulated Murine Macrophages through TAK1 Inhibition and Nrf2 Activation. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32187984/ · DOI 10.3390/ijms21062007

evidence_access

Primary abstract

experimental_model

Mouse liver dosing study.

limitations

Not evidence of universal human glutathione depletion.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

An antioxidant-associated compound can lower this defense system in a particular model.

primary_references

Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24747074/ · DOI 10.1016/j.bbrc.2014.04.039

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 452–458

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse liver dosing study. · source_derived_draft · unverified_draft

## luteolin-mouse-nrf2-gsh An antioxidant-associated compound can lower this defense system in a particular model. Luteolin reduced liver glutathione and antioxidant-enzyme expression in wild-type mice under basal and BHA-induced conditions. Model: Mouse liver dosing study. Limitations: Not evidence of universal human glutathione depletion. Evidence access: Primary abstract Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24747074/ · DOI 10.1016/j.bbrc.2014.04.039

evidence_span

{"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"}

experimental_model

HCT116 mechanism and AOM/DSS knockout-mouse experiment

exposure

Purified cinnamaldehyde cell exposure and dietary supplementation in mice

limitations

No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Mouse

plain_language

The treated wild-type mice developed less experimental colon cancer.

primary_references

[ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359

tissue_or_cell_type

Colon epithelial cancer cells and experimental inflammatory colon tumors

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 636–647

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HCT116 mechanism and AOM/DSS knockout-mouse experiment · source_derived_draft · unverified_draft

### ceylon-mouse-colon Dietary cinnamaldehyde suppressed AOM/DSS-associated colon carcinogenesis in Nrf2-intact mice. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treated wild-type mice developed less experimental colon cancer. organism: Mouse tissue_or_cell_type: Colon epithelial cancer cells and experimental inflammatory colon tumors experimental_model: HCT116 mechanism and AOM/DSS knockout-mouse experiment limitations: No human cancer-prevention outcome; the abstract identifies C151 dependence but does not resolve the transfected KEAP1 construct species. exposure: Purified cinnamaldehyde cell exposure and dietary supplementation in mice evidence_span: {"source_cache": "artifacts/ceylon-research/25712056.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd", "start_char": 0, "end_char": 1920, "text_sha256": "8ad37b0dca440e7fa609a46cf02377c2979d2be8e09291a370efb963ff3c9cfd"} [ceylon-p25712056] Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde. (2015). https://pubmed.ncbi.nlm.nih.gov/25712056/ DOI: 10.1158/1940-6207.capr-14-0359

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"}

experimental_model

Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays

exposure

Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct

limitations

Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement.

nutrient_topic

Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin

organism

Mus musculus; transfected construct species not resolved in indexed abstract

plain_language

This response required functioning Nrf2 machinery.

primary_references

[curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820

tissue_or_cell_type

JB6 epidermal cells and mouse skin

trigger_kind

machinery_impairment Imported condition classification; unverified.

Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 411–422

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays · source_derived_draft · unverified_draft

### curcumin-nrf2-loss Nrf2 siRNA abrogated curcumin-induced HO-1 expression. Condition category: machinery_impairment nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This response required functioning Nrf2 machinery. organism: Mus musculus; transfected construct species not resolved in indexed abstract tissue_or_cell_type: JB6 epidermal cells and mouse skin experimental_model: Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays limitations: Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement. exposure: Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct evidence_span: {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"} [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820

evidence_access

Primary abstract

experimental_model

Cisplatin-exposed mice; cell experiments examined antioxidant signaling.

limitations

Does not establish safe cotreatment in cancer patients or preserved antitumor efficacy.

nutrient_topic

Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine

plain_language

Protection extended to an experimental hearing injury.

primary_references

The Antioxidant Ergothioneine Alleviates Cisplatin-Induced Hearing Loss Through the Nrf2 Pathway. · 2025 · https://pubmed.ncbi.nlm.nih.gov/38770822/ · DOI 10.1089/ars.2024.0648

Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 408–414

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cisplatin-exposed mice; cell experiments examined antioxidant signaling. · source_derived_draft · unverified_draft

## ergothioneine-cochlear-defense Protection extended to an experimental hearing injury. Ergothioneine reduced cisplatin-associated auditory threshold shifts by about 30 dB in the mouse comparison. Model: Cisplatin-exposed mice; cell experiments examined antioxidant signaling. Limitations: Does not establish safe cotreatment in cancer patients or preserved antitumor efficacy. Evidence access: Primary abstract The Antioxidant Ergothioneine Alleviates Cisplatin-Induced Hearing Loss Through the Nrf2 Pathway. · 2025 · https://pubmed.ncbi.nlm.nih.gov/38770822/ · DOI 10.1089/ars.2024.0648

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Mouse-cell transcription-factor silencing.

limitations

Baseline and oxidative-stress settings are distinct.

nutrient_topic

Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

plain_language

Baseline glutathione regulation depended more on ATF4.

primary_references

Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

trigger_kind

machinery_impairment Imported condition classification; unverified.

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 120–126

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-cell transcription-factor silencing. · source_derived_draft · unverified_draft

## fisetin-atf4-basal-dependence Baseline glutathione regulation depended more on ATF4. ATF4 siRNA reduced the fisetin-associated basal glutathione increase; Nrf2 siRNA did not have the same basal requirement. Model: Mouse-cell transcription-factor silencing. Limitations: Baseline and oxidative-stress settings are distinct. Evidence access: Primary abstract Concurrent regulation of the transcription factors Nrf2 and ATF4 mediates the enhancement of glutathione levels by the flavonoid fisetin. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23618921/ · DOI 10.1016/j.bcp.2013.04.010

evidence_access

Primary abstract

experimental_model

Mouse 661W culture experiment.

limitations

Not evidence of proven human macular accumulation or clinical protection from screens.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

The tested cells tolerated a light challenge better after pretreatment.

primary_references

Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32722441/ · DOI 10.3390/md18080387

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 366–372

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse 661W culture experiment. · source_derived_draft · unverified_draft

## astaxanthin-retina-blue-light The tested cells tolerated a light challenge better after pretreatment. Astaxanthin pretreatment reduced ROS, mitochondrial injury and apoptosis after blue-light exposure in mouse 661W cells, with PI3K/Akt-Nrf2 pathway responses. Model: Mouse 661W culture experiment. Limitations: Not evidence of proven human macular accumulation or clinical protection from screens. Evidence access: Primary abstract Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32722441/ · DOI 10.3390/md18080387

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Mouse photoreceptor-derived 661W cells and pharmacological inhibitors.

limitations

Not a human diabetic-retinopathy trial; inhibitor experiments do not establish unique direct molecular targets.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

Blocking stress-response signaling removed protection in the retinal-cell model.

primary_references

Astaxanthin Protects Retinal Photoreceptor Cells against High Glucose-Induced Oxidative Stress by Induction of Antioxidant Enzymes via the PI3K/Akt/Nrf2 Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32785112/ · DOI 10.3390/antiox9080729

trigger_kind

machinery_impairment Imported condition classification; unverified.

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 358–364

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse photoreceptor-derived 661W cells and pharmacological inhibitors. · source_derived_draft · unverified_draft

## astaxanthin-retina-high-glucose Blocking stress-response signaling removed protection in the retinal-cell model. Astaxanthin reduced ROS and apoptosis in high-glucose-challenged mouse 661W cells; PI3K or Nrf2 inhibition abolished the protective effect. Model: Mouse photoreceptor-derived 661W cells and pharmacological inhibitors. Limitations: Not a human diabetic-retinopathy trial; inhibitor experiments do not establish unique direct molecular targets. Evidence access: Primary abstract Astaxanthin Protects Retinal Photoreceptor Cells against High Glucose-Induced Oxidative Stress by Induction of Antioxidant Enzymes via the PI3K/Akt/Nrf2 Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32785112/ · DOI 10.3390/antiox9080729