Nutrient chapter

Indicaxanthin

Yellow betaxanthin found in cactus pear. Its responses must not be generalized to every betalain.

69 recorded mechanisms · 1 availability situations · 2 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.

Added indicaxanthin increased resistance of beta-thalassemic red cells to peroxide-induced haemolysis.
Indicaxanthin → Oxidative haemolysis of human beta-thalassemic erythrocytes source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge
duration
Not specified in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human beta-thalassemia donor erythrocytes
limitations
Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human beta-thalassemia donor erythrocytes
plain_language
Added indicaxanthin increased resistance of beta-thalassemic red cells to peroxide-induced haemolysis.
primary_references
Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228
route
Ex vivo addition
tissue
Red blood cells
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 19–28
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human beta-thalassemia donor erythrocytes · source_derived_draft · unverified_draft
## indicaxanthin-rbc-haemolysis Added indicaxanthin increased resistance of beta-thalassemic red cells to peroxide-induced haemolysis. Model/species: Human beta-thalassemia donor erythrocytes Tissue: Red blood cells Exposure: Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge Route: Ex vivo addition Duration: Not specified in accessed abstract Limits: Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis. Primary reference: Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228 Access: Primary PubMed abstract.
Complete structured claim and evidence
Added indicaxanthin delayed vitamin E depletion during oxidative challenge of beta-thalassemic red cells.
Indicaxanthin → Vitamin E depletion in human beta-thalassemic erythrocytes source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge
duration
Not specified in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human beta-thalassemia donor erythrocytes
limitations
Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human beta-thalassemia donor erythrocytes
plain_language
Added indicaxanthin delayed vitamin E depletion during oxidative challenge of beta-thalassemic red cells.
primary_references
Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228
route
Ex vivo addition
tissue
Red blood cells
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 30–39
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human beta-thalassemia donor erythrocytes · source_derived_draft · unverified_draft
## indicaxanthin-rbc-vitamin-e Added indicaxanthin delayed vitamin E depletion during oxidative challenge of beta-thalassemic red cells. Model/species: Human beta-thalassemia donor erythrocytes Tissue: Red blood cells Exposure: Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge Route: Ex vivo addition Duration: Not specified in accessed abstract Limits: Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis. Primary reference: Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228 Access: Primary PubMed abstract.
Complete structured claim and evidence
Added indicaxanthin delayed glutathione depletion during oxidative challenge of beta-thalassemic red cells.
Indicaxanthin → Reduced glutathione depletion in human beta-thalassemic erythrocytes source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge
duration
Not specified in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human beta-thalassemia donor erythrocytes
limitations
Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human beta-thalassemia donor erythrocytes
plain_language
Added indicaxanthin delayed glutathione depletion during oxidative challenge of beta-thalassemic red cells.
primary_references
Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228
route
Ex vivo addition
tissue
Red blood cells
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 41–50
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human beta-thalassemia donor erythrocytes · source_derived_draft · unverified_draft
## indicaxanthin-rbc-glutathione Added indicaxanthin delayed glutathione depletion during oxidative challenge of beta-thalassemic red cells. Model/species: Human beta-thalassemia donor erythrocytes Tissue: Red blood cells Exposure: Indicaxanthin 1-10 micromolar; cumene hydroperoxide challenge Route: Ex vivo addition Duration: Not specified in accessed abstract Limits: Ex vivo redox protection is not demonstrated oral treatment of anemia; preservation is not proof of increased glutathione synthesis. Primary reference: Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin reduced the perferryl-haemoglobin intermediate in the spectrophotometric reaction system.
Indicaxanthin → Perferryl haemoglobin in the indicaxanthin redox assay source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin compared with Trolox and vitamin C; exact concentrations not in accessed abstract
duration
Spectrophotometric kinetic assay
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Cell-free haemoglobin redox preparation
limitations
A haemoglobin intermediate was reduced; dietary iron chelation and human treatment efficacy were not established.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Cell-free haemoglobin redox preparation
plain_language
Indicaxanthin reduced the perferryl-haemoglobin intermediate in the spectrophotometric reaction system.
primary_references
Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228
route
In vitro addition
tissue
Met-Hb/peroxide reaction mixture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 52–61
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Cell-free haemoglobin redox preparation · source_derived_draft · unverified_draft
## indicaxanthin-perferryl-hb Indicaxanthin reduced the perferryl-haemoglobin intermediate in the spectrophotometric reaction system. Model/species: Cell-free haemoglobin redox preparation Tissue: Met-Hb/peroxide reaction mixture Exposure: Indicaxanthin compared with Trolox and vitamin C; exact concentrations not in accessed abstract Route: In vitro addition Duration: Spectrophotometric kinetic assay Limits: A haemoglobin intermediate was reduced; dietary iron chelation and human treatment efficacy were not established. Primary reference: Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells. (2006). https://pubmed.ncbi.nlm.nih.gov/16984002/ DOI: 10.1080/10715760600554228 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin showed absorptive apparent permeability of 4.4 +/- 0.4 x 10^-6 cm/s in the 2013 Caco-2 transport experiment.
Indicaxanthin → Apparent indicaxanthin permeability in human Caco-2 monolayers source_derived_draftungraded
Experimental context and source evidence
dose
Dietary-consistent pigment concentrations, exact range not in accessed abstract; pH 6.0/7.4 gradient
duration
Time-course assay; exact interval not in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 epithelial monolayers on Transwell inserts
limitations
Cell permeability is not a human absorption fraction. MRP2-mediated efflux in this paper concerns betanin, not indicaxanthin. Different protocols limit comparison with the 2022 transport paper.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 epithelial monolayers on Transwell inserts
plain_language
Indicaxanthin showed absorptive apparent permeability of 4.4 +/- 0.4 x 10^-6 cm/s in the 2013 Caco-2 transport experiment.
primary_references
Trans-epithelial transport of the betalain pigments indicaxanthin and betanin across Caco-2 cell monolayers and influence of food matrix. (2013). https://pubmed.ncbi.nlm.nih.gov/22806766/ DOI: 10.1007/s00394-012-0414-5
route
In vitro transepithelial transport
tissue
Apical/basolateral compartments
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 63–72
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 epithelial monolayers on Transwell inserts · source_derived_draft · unverified_draft
## indicaxanthin-caco2-permeability Indicaxanthin showed absorptive apparent permeability of 4.4 +/- 0.4 x 10^-6 cm/s in the 2013 Caco-2 transport experiment. Model/species: Human Caco-2 epithelial monolayers on Transwell inserts Tissue: Apical/basolateral compartments Exposure: Dietary-consistent pigment concentrations, exact range not in accessed abstract; pH 6.0/7.4 gradient Route: In vitro transepithelial transport Duration: Time-course assay; exact interval not in accessed abstract Limits: Cell permeability is not a human absorption fraction. MRP2-mediated efflux in this paper concerns betanin, not indicaxanthin. Different protocols limit comparison with the 2022 transport paper. Primary reference: Trans-epithelial transport of the betalain pigments indicaxanthin and betanin across Caco-2 cell monolayers and influence of food matrix. (2013). https://pubmed.ncbi.nlm.nih.gov/22806766/ DOI: 10.1007/s00394-012-0414-5 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin transport was non-polarized and insensitive to the tested transporter inhibitors; EDTA treatment increased its passage.
Indicaxanthin → Apparent indicaxanthin permeability in human Caco-2 monolayers source_derived_draftungraded
Experimental context and source evidence
dose
Dietary-consistent pigment concentrations, exact range not in accessed abstract; pH 6.0/7.4 gradient
duration
Time-course assay; exact interval not in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 epithelial monolayers on Transwell inserts
limitations
Cell permeability is not a human absorption fraction. MRP2-mediated efflux in this paper concerns betanin, not indicaxanthin. Different protocols limit comparison with the 2022 transport paper. A paracellular contribution is supported; no specific transporter is assigned.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 epithelial monolayers on Transwell inserts
plain_language
Indicaxanthin transport was non-polarized and insensitive to the tested transporter inhibitors; EDTA treatment increased its passage.
primary_references
Trans-epithelial transport of the betalain pigments indicaxanthin and betanin across Caco-2 cell monolayers and influence of food matrix. (2013). https://pubmed.ncbi.nlm.nih.gov/22806766/ DOI: 10.1007/s00394-012-0414-5
route
In vitro transepithelial transport
tissue
Apical/basolateral compartments
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 74–83
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 epithelial monolayers on Transwell inserts · source_derived_draft · unverified_draft
## indicaxanthin-caco2-passive-transport Indicaxanthin transport was non-polarized and insensitive to the tested transporter inhibitors; EDTA treatment increased its passage. Model/species: Human Caco-2 epithelial monolayers on Transwell inserts Tissue: Apical/basolateral compartments Exposure: Dietary-consistent pigment concentrations, exact range not in accessed abstract; pH 6.0/7.4 gradient Route: In vitro transepithelial transport Duration: Time-course assay; exact interval not in accessed abstract Limits: Cell permeability is not a human absorption fraction. MRP2-mediated efflux in this paper concerns betanin, not indicaxanthin. Different protocols limit comparison with the 2022 transport paper. A paracellular contribution is supported; no specific transporter is assigned. Primary reference: Trans-epithelial transport of the betalain pigments indicaxanthin and betanin across Caco-2 cell monolayers and influence of food matrix. (2013). https://pubmed.ncbi.nlm.nih.gov/22806766/ DOI: 10.1007/s00394-012-0414-5 Access: Primary PubMed abstract.
Complete structured claim and evidence
Adding indicaxanthin reduced spontaneous contractile activity of isolated mouse ileal longitudinal muscle.
Indicaxanthin → Mouse ileal longitudinal muscle contractility source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract
duration
Acute responses; exact interval not in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Isolated mouse ileal longitudinal muscle
limitations
PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Isolated mouse ileal longitudinal muscle
plain_language
Adding indicaxanthin reduced spontaneous contractile activity of isolated mouse ileal longitudinal muscle.
primary_references
Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034
route
Ex vivo organ-bath addition
tissue
Organ-bath smooth muscle
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 85–94
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Isolated mouse ileal longitudinal muscle · source_derived_draft · unverified_draft
## indicaxanthin-ileal-contractility Adding indicaxanthin reduced spontaneous contractile activity of isolated mouse ileal longitudinal muscle. Model/species: Isolated mouse ileal longitudinal muscle Tissue: Organ-bath smooth muscle Exposure: Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract Route: Ex vivo organ-bath addition Duration: Acute responses; exact interval not in accessed abstract Limits: PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested. Primary reference: Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034 Access: Primary PubMed abstract.
Complete structured claim and evidence
Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle.
Indicaxanthin → cAMP content in mouse ileal muscle source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract
duration
Acute responses; exact interval not in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Isolated mouse ileal longitudinal muscle
limitations
PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Isolated mouse ileal longitudinal muscle
plain_language
Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle.
primary_references
Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034
route
Ex vivo organ-bath addition
tissue
Organ-bath smooth muscle
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 96–105
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Isolated mouse ileal longitudinal muscle · source_derived_draft · unverified_draft
## indicaxanthin-ileal-camp Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle. Model/species: Isolated mouse ileal longitudinal muscle Tissue: Organ-bath smooth muscle Exposure: Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract Route: Ex vivo organ-bath addition Duration: Acute responses; exact interval not in accessed abstract Limits: PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested. Primary reference: Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity.
Indicaxanthin → Forskolin-induced inhibition of mouse ileal contractility source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract
duration
Acute responses; exact interval not in accessed abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Isolated mouse ileal longitudinal muscle
limitations
PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Isolated mouse ileal longitudinal muscle
plain_language
Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity.
primary_references
Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034
route
Ex vivo organ-bath addition
tissue
Organ-bath smooth muscle
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 107–116
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Isolated mouse ileal longitudinal muscle · source_derived_draft · unverified_draft
## indicaxanthin-ileal-forskolin Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity. Model/species: Isolated mouse ileal longitudinal muscle Tissue: Organ-bath smooth muscle Exposure: Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract Route: Ex vivo organ-bath addition Duration: Acute responses; exact interval not in accessed abstract Limits: PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested. Primary reference: Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin pretreatment reduced LPS-induced microsomal PGE synthase-1 overexpression in RAW 264.7 cells.
Indicaxanthin → Mouse microsomal prostaglandin E synthase-1 / Ptges source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Mouse RAW 264.7 macrophages
limitations
High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin pretreatment reduced LPS-induced microsomal PGE synthase-1 overexpression in RAW 264.7 cells.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro pretreatment then challenge
tissue
Cellular membranes and prostaglandin pathway
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 118–127
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## indicaxanthin-macrophage-mpges Indicaxanthin pretreatment reduced LPS-induced microsomal PGE synthase-1 overexpression in RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment increased COX-2 expression in LPS-stimulated RAW 264.7 cells.
Indicaxanthin → Mouse cyclooxygenase-2 / Ptgs2 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Mouse RAW 264.7 macrophages
limitations
High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Opposite to the COX-2 response in IL-1beta-exposed human intestinal cells; different species, stimulus and concentration are retained rather than declared a contradiction.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin pretreatment increased COX-2 expression in LPS-stimulated RAW 264.7 cells.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro pretreatment then challenge
tissue
Cellular membranes and prostaglandin pathway
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 129–138
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## indicaxanthin-macrophage-cox2 Indicaxanthin pretreatment increased COX-2 expression in LPS-stimulated RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Opposite to the COX-2 response in IL-1beta-exposed human intestinal cells; different species, stimulus and concentration are retained rather than declared a contradiction. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells.
Indicaxanthin → Mouse hematopoietic prostaglandin D synthase / Hpgds source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Mouse RAW 264.7 macrophages
limitations
High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro pretreatment then challenge
tissue
Cellular membranes and prostaglandin pathway
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 140–149
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## indicaxanthin-macrophage-hpgds Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment increased production of 15-deoxy-PGJ2 in LPS-stimulated RAW 264.7 cells.
Indicaxanthin → 15-Deoxy-PGJ2 production in mouse RAW 264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Mouse RAW 264.7 macrophages
limitations
High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin pretreatment increased production of 15-deoxy-PGJ2 in LPS-stimulated RAW 264.7 cells.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro pretreatment then challenge
tissue
Cellular membranes and prostaglandin pathway
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 151–160
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## indicaxanthin-macrophage-pgj2 Indicaxanthin pretreatment increased production of 15-deoxy-PGJ2 in LPS-stimulated RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin increased early lipid hydroperoxide accumulation above the LPS-only level in RAW 264.7 cells.
Indicaxanthin → Conjugated-diene lipid hydroperoxides in mouse RAW 264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Mouse RAW 264.7 macrophages
limitations
High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin increased early lipid hydroperoxide accumulation above the LPS-only level in RAW 264.7 cells.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro pretreatment then challenge
tissue
Cellular membranes and prostaglandin pathway
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 162–171
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## indicaxanthin-macrophage-lipid-peroxides Indicaxanthin increased early lipid hydroperoxide accumulation above the LPS-only level in RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages.
Alpha-tocopherol → Prostaglandin D2 production in mouse RAW 264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 50-100 micromolar; alpha-tocopherol 100 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; lipid peroxides at 0.5 h, PGD2 at 8 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
LPS-stimulated mouse RAW 264.7 macrophages
limitations
Experimental vitamin E antagonism of this response is not evidence that vitamin E intake is harmful or that avoiding supplementation improves clinical outcomes.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
LPS-stimulated mouse RAW 264.7 macrophages
plain_language
Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro co-incubation
tissue
Membrane lipid oxidation and PGD2 production
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## indicaxanthin-vitamin-e-pgd2-antagonism Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages. Model/species: LPS-stimulated mouse RAW 264.7 macrophages Tissue: Membrane lipid oxidation and PGD2 production Exposure: Indicaxanthin 50-100 micromolar; alpha-tocopherol 100 micromolar; LPS 1 microgram/mL Route: In vitro co-incubation Duration: Indicaxanthin 1 h before LPS; lipid peroxides at 0.5 h, PGD2 at 8 h Limits: Experimental vitamin E antagonism of this response is not evidence that vitamin E intake is harmful or that avoiding supplementation improves clinical outcomes. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages.
Diphenyleneiodonium / DPI → Prostaglandin D2 production in mouse RAW 264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Indicaxanthin 50-100 micromolar; DPI 1 micromolar; LPS 1 microgram/mL
duration
Indicaxanthin 1 h before LPS; PGD2 at 8 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure
limitations
DPI is not NOX-isoform-selective; pharmacological sensitivity does not establish NOX2 necessity or a nutrient deficiency.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure
plain_language
Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages.
primary_references
Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
route
In vitro co-incubation
tissue
Redox-dependent prostaglandin pathway
trigger_kind
machinery_impairment Imported condition classification; unverified.
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## indicaxanthin-dpi-pgd2-blockade Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages. Model/species: LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure Tissue: Redox-dependent prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; DPI 1 micromolar; LPS 1 microgram/mL Route: In vitro co-incubation Duration: Indicaxanthin 1 h before LPS; PGD2 at 8 h Limits: DPI is not NOX-isoform-selective; pharmacological sensitivity does not establish NOX2 necessity or a nutrient deficiency. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
After oral indicaxanthin, rat whole-brain content peaked at 20 +/- 2.4 ng at 2.5 hours.
Indicaxanthin → Indicaxanthin exposure in rat brain source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2 micromol/kg
duration
Detected within 1 h, peak at 2.5 h, disappearance by approximately 4 h
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Rats given purified indicaxanthin
limitations
Brain exposure in rats does not demonstrate human BBB transport, clinical neuroprotection or neuronal target engagement.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Rats given purified indicaxanthin
plain_language
After oral indicaxanthin, rat whole-brain content peaked at 20 +/- 2.4 ng at 2.5 hours.
primary_references
Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612
route
Oral administration
tissue
Whole brain
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 195–204
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## indicaxanthin-rat-brain-exposure After oral indicaxanthin, rat whole-brain content peaked at 20 +/- 2.4 ng at 2.5 hours. Model/species: Rats given purified indicaxanthin Tissue: Whole brain Exposure: Indicaxanthin 2 micromol/kg Route: Oral administration Duration: Detected within 1 h, peak at 2.5 h, disappearance by approximately 4 h Limits: Brain exposure in rats does not demonstrate human BBB transport, clinical neuroprotection or neuronal target engagement. Primary reference: Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612 Access: Primary PubMed abstract.
Complete structured claim and evidence
Local indicaxanthin application reduced spontaneous firing of rat hippocampal neurons in a dose-related manner.
Indicaxanthin → Rat hippocampal neuronal firing source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 0.085-0.34 ng/neuron; glutamate challenge in selected recordings
duration
Acute firing measurements
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
In vivo rat hippocampal single-neuron recordings
limitations
Local application bypasses oral distribution. NMDAR binding was proposed by modeling, not established by this electrophysiological observation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
In vivo rat hippocampal single-neuron recordings
plain_language
Local indicaxanthin application reduced spontaneous firing of rat hippocampal neurons in a dose-related manner.
primary_references
Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612
route
Local microiontophoresis
tissue
Hippocampus
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## indicaxanthin-rat-hippocampal-firing Local indicaxanthin application reduced spontaneous firing of rat hippocampal neurons in a dose-related manner. Model/species: In vivo rat hippocampal single-neuron recordings Tissue: Hippocampus Exposure: Indicaxanthin 0.085-0.34 ng/neuron; glutamate challenge in selected recordings Route: Local microiontophoresis Duration: Acute firing measurements Limits: Local application bypasses oral distribution. NMDAR binding was proposed by modeling, not established by this electrophysiological observation. Primary reference: Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612 Access: Primary PubMed abstract.
Complete structured claim and evidence
Local indicaxanthin at 0.34 ng/neuron reduced glutamate-evoked excitation in rat hippocampal recordings.
Indicaxanthin → Glutamate-evoked excitation of rat hippocampal neurons source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 0.085-0.34 ng/neuron; glutamate challenge in selected recordings
duration
Acute firing measurements
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
In vivo rat hippocampal single-neuron recordings
limitations
Local application bypasses oral distribution. NMDAR binding was proposed by modeling, not established by this electrophysiological observation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
In vivo rat hippocampal single-neuron recordings
plain_language
Local indicaxanthin at 0.34 ng/neuron reduced glutamate-evoked excitation in rat hippocampal recordings.
primary_references
Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612
route
Local microiontophoresis
tissue
Hippocampus
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## indicaxanthin-rat-glutamate-excitation Local indicaxanthin at 0.34 ng/neuron reduced glutamate-evoked excitation in rat hippocampal recordings. Model/species: In vivo rat hippocampal single-neuron recordings Tissue: Hippocampus Exposure: Indicaxanthin 0.085-0.34 ng/neuron; glutamate challenge in selected recordings Route: Local microiontophoresis Duration: Acute firing measurements Limits: Local application bypasses oral distribution. NMDAR binding was proposed by modeling, not established by this electrophysiological observation. Primary reference: Indicaxanthin from Opuntia ficus-indica Crosses the Blood-Brain Barrier and Modulates Neuronal Bioelectric Activity in Rat Hippocampus at Dietary-Consistent Amounts. (2015). https://pubmed.ncbi.nlm.nih.gov/26227670/ DOI: 10.1021/acs.jafc.5b02612 Access: Primary PubMed abstract.
Complete structured claim and evidence
After oral indicaxanthin, pigment was detected in rat cortex, hippocampus, diencephalon, brainstem and cerebellum, but not the striato-pallidal complex.
Indicaxanthin → Indicaxanthin exposure in rat brain source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2 micromol/kg
duration
Tissue sampling 1 h after dosing
evidence_access
Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Rats given purified indicaxanthin
limitations
Measured regional distribution must not be conflated with local-injection electrophysiology; human brain exposure is unproven.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Rats given purified indicaxanthin
plain_language
After oral indicaxanthin, pigment was detected in rat cortex, hippocampus, diencephalon, brainstem and cerebellum, but not the striato-pallidal complex.
primary_references
Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133
route
Oral administration
tissue
Regional brain tissue
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## indicaxanthin-rat-regional-distribution After oral indicaxanthin, pigment was detected in rat cortex, hippocampus, diencephalon, brainstem and cerebellum, but not the striato-pallidal complex. Model/species: Rats given purified indicaxanthin Tissue: Regional brain tissue Exposure: Indicaxanthin 2 micromol/kg Route: Oral administration Duration: Tissue sampling 1 h after dosing Limits: Measured regional distribution must not be conflated with local-injection electrophysiology; human brain exposure is unproven. Primary reference: Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133 Access: Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
Complete structured claim and evidence
Local indicaxanthin reduced cortical-neuron firing at the two higher tested amounts in rats.
Indicaxanthin → Rat cortical neuronal firing source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 0.085, 0.17 and 0.34 ng/neuron
duration
Acute recording; local application for 5 min
evidence_access
Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
In vivo rat single-neuron recordings
limitations
Effects varied by region and dose. Direct striatal application produced effects even though oral-dose tissue analysis did not detect pigment there.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
In vivo rat single-neuron recordings
plain_language
Local indicaxanthin reduced cortical-neuron firing at the two higher tested amounts in rats.
primary_references
Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133
route
Local microiontophoresis
tissue
Cortex and striatum
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 239–248
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## indicaxanthin-rat-cortical-firing Local indicaxanthin reduced cortical-neuron firing at the two higher tested amounts in rats. Model/species: In vivo rat single-neuron recordings Tissue: Cortex and striatum Exposure: Indicaxanthin 0.085, 0.17 and 0.34 ng/neuron Route: Local microiontophoresis Duration: Acute recording; local application for 5 min Limits: Effects varied by region and dose. Direct striatal application produced effects even though oral-dose tissue analysis did not detect pigment there. Primary reference: Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133 Access: Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
Complete structured claim and evidence
Local indicaxanthin increased firing in rat striatal neurons, contrasting with its predominant inhibitory response in other recorded regions.
Indicaxanthin → Rat striatal neuronal firing source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 0.085, 0.17 and 0.34 ng/neuron
duration
Acute recording; local application for 5 min
evidence_access
Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
In vivo rat single-neuron recordings
limitations
Effects varied by region and dose. Direct striatal application produced effects even though oral-dose tissue analysis did not detect pigment there.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
In vivo rat single-neuron recordings
plain_language
Local indicaxanthin increased firing in rat striatal neurons, contrasting with its predominant inhibitory response in other recorded regions.
primary_references
Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133
route
Local microiontophoresis
tissue
Cortex and striatum
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 250–259
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## indicaxanthin-rat-striatal-firing Local indicaxanthin increased firing in rat striatal neurons, contrasting with its predominant inhibitory response in other recorded regions. Model/species: In vivo rat single-neuron recordings Tissue: Cortex and striatum Exposure: Indicaxanthin 0.085, 0.17 and 0.34 ng/neuron Route: Local microiontophoresis Duration: Acute recording; local application for 5 min Limits: Effects varied by region and dose. Direct striatal application produced effects even though oral-dose tissue analysis did not detect pigment there. Primary reference: Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts. (2018). https://pubmed.ncbi.nlm.nih.gov/29867444/ DOI: 10.3389/fnagi.2018.00133 Access: Primary PubMed abstract; 2018 regional neuronal results additionally inspected in PMC full text.
Complete structured claim and evidence
Yellow-cactus-pear consumption was associated with increased motor-cortex intracortical facilitation in the preliminary human study.
Cactus pear fruit meal in the 2022 neurostimulation study → Human motor-cortex intracortical facilitation source_derived_draftungraded
Experimental context and source evidence
dose
400 g yellow cactus pear fruit versus white-fruit comparator; exact indicaxanthin amount unresolved
duration
90 min after fruit; sessions separated by at least one week
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Small healthy-male neurostimulation study
limitations
Whole-food single-blind preliminary study. Methods report 12 fruit/8 comparator participants and four comparator exclusions; participant accounting and fruit-color wording have inconsistencies. No isolated-compound efficacy or cognitive benefit was demonstrated.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Small healthy-male neurostimulation study
plain_language
Yellow-cactus-pear consumption was associated with increased motor-cortex intracortical facilitation in the preliminary human study.
primary_references
Modulation of Human Motor Cortical Excitability and Plasticity by Opuntia Ficus Indica Fruit Consumption: Evidence from a Preliminary Study through Non-Invasive Brain Stimulation. (2022). https://pubmed.ncbi.nlm.nih.gov/36432601/ DOI: 10.3390/nu14224915
route
Oral whole fruit
tissue
Primary motor cortex
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 261–270
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## indicaxanthin-human-fruit-icf Yellow-cactus-pear consumption was associated with increased motor-cortex intracortical facilitation in the preliminary human study. Model/species: Small healthy-male neurostimulation study Tissue: Primary motor cortex Exposure: 400 g yellow cactus pear fruit versus white-fruit comparator; exact indicaxanthin amount unresolved Route: Oral whole fruit Duration: 90 min after fruit; sessions separated by at least one week Limits: Whole-food single-blind preliminary study. Methods report 12 fruit/8 comparator participants and four comparator exclusions; participant accounting and fruit-color wording have inconsistencies. No isolated-compound efficacy or cognitive benefit was demonstrated. Primary reference: Modulation of Human Motor Cortical Excitability and Plasticity by Opuntia Ficus Indica Fruit Consumption: Evidence from a Preliminary Study through Non-Invasive Brain Stimulation. (2022). https://pubmed.ncbi.nlm.nih.gov/36432601/ DOI: 10.3390/nu14224915 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
The six-person imaging subgroup showed no significant resting-state connectivity change after the fruit meal.
Cactus pear fruit meal in the 2022 neurostimulation study → Human resting-state fMRI connectivity source_derived_draftungraded
Experimental context and source evidence
dose
400 g yellow cactus pear
duration
Baseline and 90 min after consumption
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Six healthy participants in exploratory imaging subgroup
limitations
Small imaging subgroup; a null imaging comparison does not exclude every neural effect. Whole-fruit exposure does not isolate indicaxanthin.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Six healthy participants in exploratory imaging subgroup
plain_language
The six-person imaging subgroup showed no significant resting-state connectivity change after the fruit meal.
primary_references
Modulation of Human Motor Cortical Excitability and Plasticity by Opuntia Ficus Indica Fruit Consumption: Evidence from a Preliminary Study through Non-Invasive Brain Stimulation. (2022). https://pubmed.ncbi.nlm.nih.gov/36432601/ DOI: 10.3390/nu14224915
route
Oral whole fruit
tissue
Resting-state brain networks
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 272–281
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Six healthy participants in exploratory imaging subgroup · source_derived_draft · unverified_draft
## indicaxanthin-human-fruit-fmri-null The six-person imaging subgroup showed no significant resting-state connectivity change after the fruit meal. Model/species: Six healthy participants in exploratory imaging subgroup Tissue: Resting-state brain networks Exposure: 400 g yellow cactus pear Route: Oral whole fruit Duration: Baseline and 90 min after consumption Limits: Small imaging subgroup; a null imaging comparison does not exclude every neural effect. Whole-fruit exposure does not isolate indicaxanthin. Primary reference: Modulation of Human Motor Cortical Excitability and Plasticity by Opuntia Ficus Indica Fruit Consumption: Evidence from a Preliminary Study through Non-Invasive Brain Stimulation. (2022). https://pubmed.ncbi.nlm.nih.gov/36432601/ DOI: 10.3390/nu14224915 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone.
Indicaxanthin → Apoptosis in human HeLa cervical cancer cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
duration
24 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human HeLa cervical cancer cells
limitations
Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human HeLa cervical cancer cells
plain_language
Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone.
primary_references
The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
route
In vitro co-treatment
tissue
Cell death and redox assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 283–292
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-cisplatin-apoptosis Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells.
Indicaxanthin → Reduced glutathione-associated signal in human HeLa cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
duration
24 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human HeLa cervical cancer cells
limitations
Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Glutathione was assessed with CMFDA fluorescence; the result does not establish an isolated block of synthesis.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human HeLa cervical cancer cells
plain_language
Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells.
primary_references
The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
route
In vitro co-treatment
tissue
Cell death and redox assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 294–303
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-cisplatin-gsh Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Glutathione was assessed with CMFDA fluorescence; the result does not establish an isolated block of synthesis. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells.
Indicaxanthin → Oxidant-sensitive fluorescence in human HeLa cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
duration
24 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human HeLa cervical cancer cells
limitations
Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human HeLa cervical cancer cells
plain_language
Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells.
primary_references
The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
route
In vitro co-treatment
tissue
Cell death and redox assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 305–314
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-cisplatin-ros Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment.
Indicaxanthin → Viability of human HeLa cervical cancer cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2, 5 or 10 micromolar plus a cisplatin concentration series
duration
24 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human HeLa cervical cancer cells
limitations
Lower indicaxanthin concentrations were examined in a separate viability experiment; do not transfer all high-dose mechanistic measurements to this range.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human HeLa cervical cancer cells
plain_language
Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment.
primary_references
The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
route
In vitro co-treatment
tissue
Viability assay
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 316–325
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-cisplatin-low-dose Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment. Model/species: Human HeLa cervical cancer cells Tissue: Viability assay Exposure: Indicaxanthin 2, 5 or 10 micromolar plus a cisplatin concentration series Route: In vitro co-treatment Duration: 24 h Limits: Lower indicaxanthin concentrations were examined in a separate viability experiment; do not transfer all high-dose mechanistic measurements to this range. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells.
N-Acetyl-L-cysteine → Apoptosis in human HeLa cervical cancer cells source_derived_draftungraded
Experimental context and source evidence
dose
N-acetylcysteine 2 mM before indicaxanthin 60 micromolar plus cisplatin 10 micromolar
duration
NAC 1 h before the 24 h combination exposure
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human HeLa cervical cancer cells with NAC pretreatment
limitations
NAC blunted the combination response without restoring every outcome to baseline. This experiment is not a recommendation for or against NAC during chemotherapy.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human HeLa cervical cancer cells with NAC pretreatment
plain_language
N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells.
primary_references
The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
route
In vitro pretreatment/co-treatment
tissue
Cell death and redox assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 327–336
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells with NAC pretreatment · source_derived_draft · unverified_draft
## indicaxanthin-nac-combination-antagonism N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells. Model/species: Human HeLa cervical cancer cells with NAC pretreatment Tissue: Cell death and redox assays Exposure: N-acetylcysteine 2 mM before indicaxanthin 60 micromolar plus cisplatin 10 micromolar Route: In vitro pretreatment/co-treatment Duration: NAC 1 h before the 24 h combination exposure Limits: NAC blunted the combination response without restoring every outcome to baseline. This experiment is not a recommendation for or against NAC during chemotherapy. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs.
Indicaxanthin → NF-kappaB transcriptional activity in human HUVECs source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
duration
1 h pretreatment followed by 16 h oxidized-LDL exposure
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human umbilical vein endothelial cells / HUVECs
limitations
Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human umbilical vein endothelial cells / HUVECs
plain_language
Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs.
primary_references
Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
route
In vitro pretreatment and challenge
tissue
Endothelial culture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 338–347
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft
## indicaxanthin-endothelial-nfkb Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment prevented the oxidized-LDL-associated decrease in ABCA1 mRNA and protein in HUVECs.
Indicaxanthin → Human ATP-binding cassette transporter A1 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
duration
1 h pretreatment followed by 16 h oxidized-LDL exposure
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human umbilical vein endothelial cells / HUVECs
limitations
Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human umbilical vein endothelial cells / HUVECs
plain_language
Indicaxanthin pretreatment prevented the oxidized-LDL-associated decrease in ABCA1 mRNA and protein in HUVECs.
primary_references
Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
route
In vitro pretreatment and challenge
tissue
Endothelial culture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 349–358
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft
## indicaxanthin-endothelial-abca1 Indicaxanthin pretreatment prevented the oxidized-LDL-associated decrease in ABCA1 mRNA and protein in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 mRNA and protein increases in HUVECs.
Indicaxanthin → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
duration
1 h pretreatment followed by 16 h oxidized-LDL exposure
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human umbilical vein endothelial cells / HUVECs
limitations
Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human umbilical vein endothelial cells / HUVECs
plain_language
Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 mRNA and protein increases in HUVECs.
primary_references
Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
route
In vitro pretreatment and challenge
tissue
Endothelial culture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 360–369
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft
## indicaxanthin-endothelial-icam1 Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 mRNA and protein increases in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs.
Indicaxanthin → Human vascular cell adhesion molecule 1 / VCAM1 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
duration
1 h pretreatment followed by 16 h oxidized-LDL exposure
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human umbilical vein endothelial cells / HUVECs
limitations
Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human umbilical vein endothelial cells / HUVECs
plain_language
Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs.
primary_references
Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
route
In vitro pretreatment and challenge
tissue
Endothelial culture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 371–380
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft
## indicaxanthin-endothelial-vcam1 Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells.
Indicaxanthin → p16INK4a promoter methylation in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract
duration
Exposure duration not specified in the accessed primary abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Proliferating human Caco-2 colorectal cancer cells
limitations
Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Proliferating human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells.
primary_references
Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029
route
In vitro addition
tissue
Epigenetic and growth assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 382–391
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Proliferating human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-p16-promoter Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells. Model/species: Proliferating human Caco-2 colorectal cancer cells Tissue: Epigenetic and growth assays Exposure: Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract Route: In vitro addition Duration: Exposure duration not specified in the accessed primary abstract Limits: Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people. Primary reference: Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells.
Indicaxanthin → Human CDKN2A p16INK4a isoform source_derived_draftungraded
Experimental context and source evidence
dose
Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract
duration
Exposure duration not specified in the accessed primary abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Proliferating human Caco-2 colorectal cancer cells
limitations
Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Proliferating human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells.
primary_references
Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029
route
In vitro addition
tissue
Epigenetic and growth assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 393–402
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Proliferating human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-p16-expression Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells. Model/species: Proliferating human Caco-2 colorectal cancer cells Tissue: Epigenetic and growth assays Exposure: Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract Route: In vitro addition Duration: Exposure duration not specified in the accessed primary abstract Limits: Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people. Primary reference: Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029 Access: Primary PubMed abstract.
Complete structured claim and evidence
Purified indicaxanthin inhibited proliferating Caco-2-cell growth, with a reported IC50 of 115 +/- 15 micromolar.
Indicaxanthin → Proliferation of human Caco-2 cancer cells source_derived_draftungraded
Experimental context and source evidence
dose
Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract
duration
Exposure duration not specified in the accessed primary abstract
evidence_access
Primary PubMed abstract.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Proliferating human Caco-2 colorectal cancer cells
limitations
Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Proliferating human Caco-2 colorectal cancer cells
plain_language
Purified indicaxanthin inhibited proliferating Caco-2-cell growth, with a reported IC50 of 115 +/- 15 micromolar.
primary_references
Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029
route
In vitro addition
tissue
Epigenetic and growth assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 404–413
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Proliferating human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-caco2-growth Purified indicaxanthin inhibited proliferating Caco-2-cell growth, with a reported IC50 of 115 +/- 15 micromolar. Model/species: Proliferating human Caco-2 colorectal cancer cells Tissue: Epigenetic and growth assays Exposure: Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract Route: In vitro addition Duration: Exposure duration not specified in the accessed primary abstract Limits: Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people. Primary reference: Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029 Access: Primary PubMed abstract.
Complete structured claim and evidence
Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells.
Indicaxanthin → LC3-II abundance in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 10, 50 and 100 micromolar
duration
48 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 colorectal cancer cells
limitations
Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells.
primary_references
Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495
route
In vitro addition
tissue
Autophagy markers and DNA methylome
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 415–424
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-autophagy-lc3 Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells. Model/species: Human Caco-2 colorectal cancer cells Tissue: Autophagy markers and DNA methylome Exposure: Indicaxanthin 10, 50 and 100 micromolar Route: In vitro addition Duration: 48 h Limits: Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. Primary reference: Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin at 50 micromolar increased Beclin1 protein abundance in Caco-2 cells.
Indicaxanthin → Human Beclin 1 / BECN1 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 10, 50 and 100 micromolar
duration
48 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 colorectal cancer cells
limitations
Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. The protein response was not monotonic across the tested concentrations.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin at 50 micromolar increased Beclin1 protein abundance in Caco-2 cells.
primary_references
Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495
route
In vitro addition
tissue
Autophagy markers and DNA methylome
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 426–435
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-autophagy-becn1 Indicaxanthin at 50 micromolar increased Beclin1 protein abundance in Caco-2 cells. Model/species: Human Caco-2 colorectal cancer cells Tissue: Autophagy markers and DNA methylome Exposure: Indicaxanthin 10, 50 and 100 micromolar Route: In vitro addition Duration: 48 h Limits: Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. The protein response was not monotonic across the tested concentrations. Primary reference: Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin at 50 or 100 micromolar increased acidic-vesicle fluorescence in Caco-2 cells.
Indicaxanthin → Acidic vesicular organelles in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 10, 50 and 100 micromolar
duration
48 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 colorectal cancer cells
limitations
Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin at 50 or 100 micromolar increased acidic-vesicle fluorescence in Caco-2 cells.
primary_references
Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495
route
In vitro addition
tissue
Autophagy markers and DNA methylome
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 437–446
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-autophagy-organelles Indicaxanthin at 50 or 100 micromolar increased acidic-vesicle fluorescence in Caco-2 cells. Model/species: Human Caco-2 colorectal cancer cells Tissue: Autophagy markers and DNA methylome Exposure: Indicaxanthin 10, 50 and 100 micromolar Route: In vitro addition Duration: 48 h Limits: Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. Primary reference: Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin treatment shifted the Caco-2 RRBS profile toward greater genomic CpG methylation, most strongly at 50 micromolar.
Indicaxanthin → Genomic CpG methylation in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 10, 50 and 100 micromolar
duration
48 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 colorectal cancer cells
limitations
Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 colorectal cancer cells
plain_language
Indicaxanthin treatment shifted the Caco-2 RRBS profile toward greater genomic CpG methylation, most strongly at 50 micromolar.
primary_references
Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495
route
In vitro addition
tissue
Autophagy markers and DNA methylome
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 448–457
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-global-methylation Indicaxanthin treatment shifted the Caco-2 RRBS profile toward greater genomic CpG methylation, most strongly at 50 micromolar. Model/species: Human Caco-2 colorectal cancer cells Tissue: Autophagy markers and DNA methylome Exposure: Indicaxanthin 10, 50 and 100 micromolar Route: In vitro addition Duration: 48 h Limits: Marker abundance and acidic organelles are not sufficient alone to quantify complete autophagic flux. Predicted BCL2 binding remains computational; methylation associations do not prove causation. Primary reference: Indicaxanthin Induces Autophagy in Intestinal Epithelial Cancer Cells by Epigenetic Mechanisms Involving DNA Methylation. (2023). https://pubmed.ncbi.nlm.nih.gov/37571432/ DOI: 10.3390/nu15153495 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
The 2025 Caco-2 methylome analysis associated indicaxanthin exposure with increased methylation at rDNA loci.
Indicaxanthin → rDNA-locus methylation in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 10 and 50 micromolar analysis; study also includes 100 micromolar
duration
48 h
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Human Caco-2 colorectal cancer cells; RRBS analysis
limitations
Same research program and related RRBS methods as the 2023 study; independent dataset replication is not established. rDNA methylation is not direct proof of reduced ribosome production or cell transdifferentiation.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Human Caco-2 colorectal cancer cells; RRBS analysis
plain_language
The 2025 Caco-2 methylome analysis associated indicaxanthin exposure with increased methylation at rDNA loci.
primary_references
Epigenetic Remodeling of Regulatory Regions by Indicaxanthin Suggests a Shift in Cell Identity Programs in Colorectal Cancer Cells. (2025). https://pubmed.ncbi.nlm.nih.gov/40649850/ DOI: 10.3390/ijms26136072
route
In vitro treatment and methylome analysis
tissue
rDNA loci and regulatory DNA
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 459–468
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human Caco-2 colorectal cancer cells; RRBS analysis · source_derived_draft · unverified_draft
## indicaxanthin-rdna-methylation The 2025 Caco-2 methylome analysis associated indicaxanthin exposure with increased methylation at rDNA loci. Model/species: Human Caco-2 colorectal cancer cells; RRBS analysis Tissue: rDNA loci and regulatory DNA Exposure: Indicaxanthin 10 and 50 micromolar analysis; study also includes 100 micromolar Route: In vitro treatment and methylome analysis Duration: 48 h Limits: Same research program and related RRBS methods as the 2023 study; independent dataset replication is not established. rDNA methylation is not direct proof of reduced ribosome production or cell transdifferentiation. Primary reference: Epigenetic Remodeling of Regulatory Regions by Indicaxanthin Suggests a Shift in Cell Identity Programs in Colorectal Cancer Cells. (2025). https://pubmed.ncbi.nlm.nih.gov/40649850/ DOI: 10.3390/ijms26136072 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Oral indicaxanthin reduced cortical TUNEL-positive cells in high-fat-diet-fed male mice.
Indicaxanthin → Cortical TUNEL-positive cells in high-fat-diet-fed mice source_derived_draftungraded
Experimental context and source evidence
dose
High-fat diet for 10 weeks then indicaxanthin for 4 weeks; abstract reports 0.86 mg/kg/day, methods state 0.4 mg/kg twice daily
duration
4 treatment weeks; eight mice/group
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Male mice with diet-induced obesity
limitations
Dose wording differs between abstract and methods and is preserved unresolved. Changes in microbial abundance do not demonstrate measured SCFA production or microbiota-mediated causation of brain changes. Article assigned 2026 issue; earlier online indexing retained in PubMed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Male mice with diet-induced obesity
plain_language
Oral indicaxanthin reduced cortical TUNEL-positive cells in high-fat-diet-fed male mice.
primary_references
Positive impact of indicaxanthin from Opuntia ficus-indica fruit on high-fat diet-induced neuronal damage and gut microbiota dysbiosis. (2026). https://pubmed.ncbi.nlm.nih.gov/39314163/ DOI: 10.4103/NRR.NRR-D-23-02039
route
Oral indicaxanthin in water
tissue
Cerebral cortex and gut microbiota
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 470–479
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Male mice with diet-induced obesity · source_derived_draft · unverified_draft
## indicaxanthin-hfd-cortical-cell-death Oral indicaxanthin reduced cortical TUNEL-positive cells in high-fat-diet-fed male mice. Model/species: Male mice with diet-induced obesity Tissue: Cerebral cortex and gut microbiota Exposure: High-fat diet for 10 weeks then indicaxanthin for 4 weeks; abstract reports 0.86 mg/kg/day, methods state 0.4 mg/kg twice daily Route: Oral indicaxanthin in water Duration: 4 treatment weeks; eight mice/group Limits: Dose wording differs between abstract and methods and is preserved unresolved. Changes in microbial abundance do not demonstrate measured SCFA production or microbiota-mediated causation of brain changes. Article assigned 2026 issue; earlier online indexing retained in PubMed. Primary reference: Positive impact of indicaxanthin from Opuntia ficus-indica fruit on high-fat diet-induced neuronal damage and gut microbiota dysbiosis. (2026). https://pubmed.ncbi.nlm.nih.gov/39314163/ DOI: 10.4103/NRR.NRR-D-23-02039 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Oral indicaxanthin altered gut microbial relative abundances in high-fat-diet-fed male mice.
Indicaxanthin → Gut microbial composition in high-fat-diet-fed mice source_derived_draftungraded
Experimental context and source evidence
dose
High-fat diet for 10 weeks then indicaxanthin for 4 weeks; abstract reports 0.86 mg/kg/day, methods state 0.4 mg/kg twice daily
duration
4 treatment weeks; eight mice/group
evidence_access
Primary open full text, relevant results/methods and PubMed metadata.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Male mice with diet-induced obesity
limitations
Dose wording differs between abstract and methods and is preserved unresolved. Changes in microbial abundance do not demonstrate measured SCFA production or microbiota-mediated causation of brain changes. Article assigned 2026 issue; earlier online indexing retained in PubMed.
nutrient_topic
Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
organism
Male mice with diet-induced obesity
plain_language
Oral indicaxanthin altered gut microbial relative abundances in high-fat-diet-fed male mice.
primary_references
Positive impact of indicaxanthin from Opuntia ficus-indica fruit on high-fat diet-induced neuronal damage and gut microbiota dysbiosis. (2026). https://pubmed.ncbi.nlm.nih.gov/39314163/ DOI: 10.4103/NRR.NRR-D-23-02039
route
Oral indicaxanthin in water
tissue
Cerebral cortex and gut microbiota
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 481–490
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Male mice with diet-induced obesity · source_derived_draft · unverified_draft
## indicaxanthin-hfd-microbiota Oral indicaxanthin altered gut microbial relative abundances in high-fat-diet-fed male mice. Model/species: Male mice with diet-induced obesity Tissue: Cerebral cortex and gut microbiota Exposure: High-fat diet for 10 weeks then indicaxanthin for 4 weeks; abstract reports 0.86 mg/kg/day, methods state 0.4 mg/kg twice daily Route: Oral indicaxanthin in water Duration: 4 treatment weeks; eight mice/group Limits: Dose wording differs between abstract and methods and is preserved unresolved. Changes in microbial abundance do not demonstrate measured SCFA production or microbiota-mediated causation of brain changes. Article assigned 2026 issue; earlier online indexing retained in PubMed. Primary reference: Positive impact of indicaxanthin from Opuntia ficus-indica fruit on high-fat diet-induced neuronal damage and gut microbiota dysbiosis. (2026). https://pubmed.ncbi.nlm.nih.gov/39314163/ DOI: 10.4103/NRR.NRR-D-23-02039 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidence
Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta.
Indicaxanthin → Epithelial permeability of human Caco-2 monolayers source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 317–325
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-barrier Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells.
Indicaxanthin → Cyclooxygenase-2 (PTGS2) source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 277–285
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-cox2 Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.
Indicaxanthin → NF-kappaB activation in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 267–275
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-nfkb Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells.
Indicaxanthin → Human inducible nitric oxide synthase / iNOS / NOS2 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 287–295
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-nos2 Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.
Indicaxanthin → Human NADPH oxidase 1 / NOX1 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 257–265
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-nox1 Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.
Indicaxanthin → Reactive oxygen species generation in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 297–305
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-ros Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols.
Indicaxanthin → Total thiol content in human Caco-2 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
duration
24 h for mediator release and permeability; earlier signaling assays
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Differentiated human Caco-2 intestinal epithelial monolayers
limitations
No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Differentiated human Caco-2 intestinal epithelial monolayers
plain_language
Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols.
primary_references
Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
route
In vitro co-incubation
tissue
Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 307–315
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-thiols Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.
Cactus pear pulp in the 2004 betalain pharmacokinetic study → Copper-driven LDL oxidation source_derived_draftungraded
Experimental context and source evidence
dose
Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin
duration
Plasma/urine followed for 12 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Eight healthy human volunteers
limitations
Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Eight healthy human volunteers
plain_language
LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.
primary_references
Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
route
Oral whole food
tissue
Plasma, urine and isolated LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 517–525
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Eight healthy human volunteers · source_derived_draft · unverified_draft
## betalains-human-food-ldl LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged. Model/species: Eight healthy human volunteers Tissue: Plasma, urine and isolated LDL Exposure: Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin Route: Oral whole food Duration: Plasma/urine followed for 12 h Limits: Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption. Primary reference: Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
Complete structured claim and evidence
Indicaxanthin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed.
Indicaxanthin → Human myeloperoxidase / MPO source_derived_draftungraded
Experimental context and source evidence
dose
Micromolar substrates; concentration-dependent chlorination assays
duration
Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Purified human myeloperoxidase; cell-free chemistry
limitations
MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Purified human myeloperoxidase; cell-free chemistry
plain_language
Indicaxanthin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed.
primary_references
Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
route
In vitro reagent addition
tissue
MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 177–185
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-indicaxanthin-chlorination Indicaxanthin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidence
Indicaxanthin reacted directly with hypochlorous acid in the kinetic assay.
Indicaxanthin → Hypochlorous acid / HOCl source_derived_draftungraded
Experimental context and source evidence
dose
Micromolar substrates; concentration-dependent chlorination assays
duration
Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Purified human myeloperoxidase; cell-free chemistry
limitations
MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Purified human myeloperoxidase; cell-free chemistry
plain_language
Indicaxanthin reacted directly with hypochlorous acid in the kinetic assay.
primary_references
Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
route
In vitro reagent addition
tissue
MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 167–175
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-indicaxanthin-hocl Indicaxanthin reacted directly with hypochlorous acid in the kinetic assay. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidence
After cactus pear ingestion, plasma indicaxanthin peaked at 3 h and was undetectable by 12 h.
Cactus pear pulp in the 2004 betalain pharmacokinetic study → Human plasma indicaxanthin exposure source_derived_draftungraded
Experimental context and source evidence
dose
Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin
duration
Plasma/urine followed for 12 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Eight healthy human volunteers
limitations
Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Eight healthy human volunteers
plain_language
After cactus pear ingestion, plasma indicaxanthin peaked at 3 h and was undetectable by 12 h.
primary_references
Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
route
Oral whole food
tissue
Plasma, urine and isolated LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 507–515
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Eight healthy human volunteers · source_derived_draft · unverified_draft
## betalains-indicaxanthin-human-pk After cactus pear ingestion, plasma indicaxanthin peaked at 3 h and was undetectable by 12 h. Model/species: Eight healthy human volunteers Tissue: Plasma, urine and isolated LDL Exposure: Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin Route: Oral whole food Duration: Plasma/urine followed for 12 h Limits: Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption. Primary reference: Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
Complete structured claim and evidence
Adding indicaxanthin to human plasma produced pigment-enriched LDL after particle isolation.
Indicaxanthin → Low-density lipoprotein particles; preparation specified source_derived_draftungraded
Experimental context and source evidence
dose
25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
duration
Kinetic oxidation assay; incubation duration not specified in accessed abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human pooled plasma from 10 healthy donors; isolated LDL
limitations
Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human pooled plasma from 10 healthy donors; isolated LDL
plain_language
Adding indicaxanthin to human plasma produced pigment-enriched LDL after particle isolation.
primary_references
Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
route
Ex vivo spiking, not oral dosing
tissue
Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 67–75
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-indicaxanthin-ldl-binding Adding indicaxanthin to human plasma produced pigment-enriched LDL after particle isolation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidence
LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation.
Indicaxanthin → Copper-driven LDL oxidation source_derived_draftungraded
Experimental context and source evidence
dose
25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
duration
Kinetic oxidation assay; incubation duration not specified in accessed abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human pooled plasma from 10 healthy donors; isolated LDL
limitations
Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human pooled plasma from 10 healthy donors; isolated LDL
plain_language
LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation.
primary_references
Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
route
Ex vivo spiking, not oral dosing
tissue
Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 77–85
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-indicaxanthin-ldl-oxidation LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidence
Indicaxanthin lowered NOX2 mRNA in the stimulated murine macrophage comparison.
Indicaxanthin → Mouse CYBB / gp91phox source_derived_draftungraded
Experimental context and source evidence
dose
Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge
duration
Not specified in accessed primary abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Mouse RAW 264.7 macrophages
limitations
Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Transcript measurement; not direct enzyme inhibition.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin lowered NOX2 mRNA in the stimulated murine macrophage comparison.
primary_references
Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
route
In vitro exposure
tissue
Macrophages
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 407–415
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## betalains-indicaxanthin-mouse-nox2 Indicaxanthin lowered NOX2 mRNA in the stimulated murine macrophage comparison. Model/species: Mouse RAW 264.7 macrophages Tissue: Macrophages Exposure: Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Transcript measurement; not direct enzyme inhibition. Primary reference: Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
Complete structured claim and evidence
Indicaxanthin increased ROS beyond the hydrogen-peroxide-challenged level in RAW 264.7 cells.
Indicaxanthin → Reactive oxygen species generation in mouse RAW 264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
dose
Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge
duration
Not specified in accessed primary abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Mouse RAW 264.7 macrophages
limitations
Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Context difference from intestinal anti-inflammatory findings; not a contradiction or a universal pigment property.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Mouse RAW 264.7 macrophages
plain_language
Indicaxanthin increased ROS beyond the hydrogen-peroxide-challenged level in RAW 264.7 cells.
primary_references
Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
route
In vitro exposure
tissue
Macrophages
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 437–445
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## betalains-indicaxanthin-mouse-prooxidant Indicaxanthin increased ROS beyond the hydrogen-peroxide-challenged level in RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Macrophages Exposure: Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Context difference from intestinal anti-inflammatory findings; not a contradiction or a universal pigment property. Primary reference: Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
Complete structured claim and evidence
Indicaxanthin donated one electron to MPO compound I, producing compound II.
Indicaxanthin → Human myeloperoxidase compound I source_derived_draftungraded
Experimental context and source evidence
dose
Micromolar substrates; concentration-dependent chlorination assays
duration
Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Purified human myeloperoxidase; cell-free chemistry
limitations
MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound I, not overall inhibition of MPO.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Purified human myeloperoxidase; cell-free chemistry
plain_language
Indicaxanthin donated one electron to MPO compound I, producing compound II.
primary_references
Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
route
In vitro reagent addition
tissue
MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 147–155
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-indicaxanthin-mpo-i Indicaxanthin donated one electron to MPO compound I, producing compound II. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound I, not overall inhibition of MPO. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidence
Indicaxanthin reduced MPO compound II to the native ferric enzyme.
Indicaxanthin → Human myeloperoxidase compound II source_derived_draftungraded
Experimental context and source evidence
dose
Micromolar substrates; concentration-dependent chlorination assays
duration
Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Purified human myeloperoxidase; cell-free chemistry
limitations
MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound II; this step can restore chlorination activity.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Purified human myeloperoxidase; cell-free chemistry
plain_language
Indicaxanthin reduced MPO compound II to the native ferric enzyme.
primary_references
Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
route
In vitro reagent addition
tissue
MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 157–165
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-indicaxanthin-mpo-ii Indicaxanthin reduced MPO compound II to the native ferric enzyme. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound II; this step can restore chlorination activity. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidence
Indicaxanthin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s.
Indicaxanthin → Apparent indicaxanthin permeability in human Caco-2 monolayers source_derived_draftungraded
Experimental context and source evidence
dose
Betalains 5-80 micromolar
duration
Not specified in accessed primary abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human Caco-2 intestinal epithelial cell model
limitations
Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. The range spans the three compounds; it is not an assigned compound-specific coefficient.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human Caco-2 intestinal epithelial cell model
plain_language
Indicaxanthin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s.
primary_references
Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
route
In vitro exposure
tissue
Intestinal cells and monolayer transport
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 377–385
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human Caco-2 intestinal epithelial cell model · source_derived_draft · unverified_draft
## betalains-indicaxanthin-transport Indicaxanthin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s. Model/species: Human Caco-2 intestinal epithelial cell model Tissue: Intestinal cells and monolayer transport Exposure: Betalains 5-80 micromolar Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. The range spans the three compounds; it is not an assigned compound-specific coefficient. Primary reference: Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
Complete structured claim and evidence
Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action.
Indicaxanthin → LDL vitamin E consumption during oxidation source_derived_draftungraded
Experimental context and source evidence
dose
25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
duration
Kinetic oxidation assay; incubation duration not specified in accessed abstract
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human pooled plasma from 10 healthy donors; isolated LDL
limitations
Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. The authors infer assay synergy; direct tocopheroxyl-radical recycling is not established.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human pooled plasma from 10 healthy donors; isolated LDL
plain_language
Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action.
primary_references
Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
route
Ex vivo spiking, not oral dosing
tissue
Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 87–95
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-indicaxanthin-vitamin-e Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. The authors infer assay synergy; direct tocopheroxyl-radical recycling is not established. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidence
Indicaxanthin reduced ATP depletion during smoke-extract exposure of isolated red cells.
Indicaxanthin → Human erythrocyte ATP content source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract
duration
3 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human isolated red blood cells challenged with cigarette smoke extract
limitations
An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human isolated red blood cells challenged with cigarette smoke extract
plain_language
Indicaxanthin reduced ATP depletion during smoke-extract exposure of isolated red cells.
primary_references
Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
route
Ex vivo co-incubation
tissue
Erythrocyte membrane and cytosol
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 477–485
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human isolated red blood cells challenged with cigarette smoke extract · source_derived_draft · unverified_draft
## betalains-redcell-atp Indicaxanthin reduced ATP depletion during smoke-extract exposure of isolated red cells. Model/species: Human isolated red blood cells challenged with cigarette smoke extract Tissue: Erythrocyte membrane and cytosol Exposure: Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract Route: Ex vivo co-incubation Duration: 3 h Limits: An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract. Primary reference: Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
Complete structured claim and evidence
Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells.
Indicaxanthin → Human caspase-3 / CASP3 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract
duration
3 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human isolated red blood cells challenged with cigarette smoke extract
limitations
An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human isolated red blood cells challenged with cigarette smoke extract
plain_language
Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells.
primary_references
Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
route
Ex vivo co-incubation
tissue
Erythrocyte membrane and cytosol
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 467–475
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human isolated red blood cells challenged with cigarette smoke extract · source_derived_draft · unverified_draft
## betalains-redcell-casp3 Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells. Model/species: Human isolated red blood cells challenged with cigarette smoke extract Tissue: Erythrocyte membrane and cytosol Exposure: Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract Route: Ex vivo co-incubation Duration: 3 h Limits: An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract. Primary reference: Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
Complete structured claim and evidence
Indicaxanthin prevented smoke-extract-triggered Fas aggregation and recruitment of FADD and caspase-8 at erythrocyte membranes.
Indicaxanthin → Fas death-inducing signaling complex in human erythrocytes source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract
duration
3 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human isolated red blood cells challenged with cigarette smoke extract
limitations
An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human isolated red blood cells challenged with cigarette smoke extract
plain_language
Indicaxanthin prevented smoke-extract-triggered Fas aggregation and recruitment of FADD and caspase-8 at erythrocyte membranes.
primary_references
Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
route
Ex vivo co-incubation
tissue
Erythrocyte membrane and cytosol
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 457–465
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human isolated red blood cells challenged with cigarette smoke extract · source_derived_draft · unverified_draft
## betalains-redcell-disc Indicaxanthin prevented smoke-extract-triggered Fas aggregation and recruitment of FADD and caspase-8 at erythrocyte membranes. Model/species: Human isolated red blood cells challenged with cigarette smoke extract Tissue: Erythrocyte membrane and cytosol Exposure: Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract Route: Ex vivo co-incubation Duration: 3 h Limits: An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract. Primary reference: Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
Complete structured claim and evidence
Indicaxanthin reduced smoke-extract-induced phosphatidylserine externalization.
Indicaxanthin → Human erythrocyte surface phosphatidylserine exposure source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract
duration
3 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human isolated red blood cells challenged with cigarette smoke extract
limitations
An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human isolated red blood cells challenged with cigarette smoke extract
plain_language
Indicaxanthin reduced smoke-extract-induced phosphatidylserine externalization.
primary_references
Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
route
Ex vivo co-incubation
tissue
Erythrocyte membrane and cytosol
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 487–495
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human isolated red blood cells challenged with cigarette smoke extract · source_derived_draft · unverified_draft
## betalains-redcell-ps Indicaxanthin reduced smoke-extract-induced phosphatidylserine externalization. Model/species: Human isolated red blood cells challenged with cigarette smoke extract Tissue: Erythrocyte membrane and cytosol Exposure: Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract Route: Ex vivo co-incubation Duration: 3 h Limits: An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract. Primary reference: Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051
Complete structured claim and evidence
Co-incubating 2.5 micromolar indicaxanthin prevented the measured 7-ketocholesterol-induced pro-apoptotic events.
Indicaxanthin → 7-Ketocholesterol-induced apoptosis in human THP-1 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract
duration
Kinetic observations within 24 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
limitations
Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
plain_language
Co-incubating 2.5 micromolar indicaxanthin prevented the measured 7-ketocholesterol-induced pro-apoptotic events.
primary_references
Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
route
In vitro co-incubation
tissue
Myeloid cells; cytosol and mitochondria
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 347–355
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol · source_derived_draft · unverified_draft
## betalains-thp1-apoptosis Co-incubating 2.5 micromolar indicaxanthin prevented the measured 7-ketocholesterol-induced pro-apoptotic events. Model/species: Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol Tissue: Myeloid cells; cytosol and mitochondria Exposure: Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract Route: In vitro co-incubation Duration: Kinetic observations within 24 h Limits: Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested. Primary reference: Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
Complete structured claim and evidence
Indicaxanthin preserved cytosolic calcium homeostasis during the 7-ketocholesterol challenge.
Indicaxanthin → Cytosolic calcium in human THP-1 cells source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract
duration
Kinetic observations within 24 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
limitations
Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
plain_language
Indicaxanthin preserved cytosolic calcium homeostasis during the 7-ketocholesterol challenge.
primary_references
Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
route
In vitro co-incubation
tissue
Myeloid cells; cytosol and mitochondria
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 337–345
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol · source_derived_draft · unverified_draft
## betalains-thp1-calcium Indicaxanthin preserved cytosolic calcium homeostasis during the 7-ketocholesterol challenge. Model/species: Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol Tissue: Myeloid cells; cytosol and mitochondria Exposure: Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract Route: In vitro co-incubation Duration: Kinetic observations within 24 h Limits: Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested. Primary reference: Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
Complete structured claim and evidence
Indicaxanthin prevented 7-ketocholesterol-associated NOX4 overexpression in THP-1 cells.
Indicaxanthin → Human NADPH oxidase 4 / NOX4 source_derived_draftungraded
Experimental context and source evidence
dose
Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract
duration
Kinetic observations within 24 h
evidence_access
Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
evidence_scope
literature_reviewed; source-derived curation, not universally established human effects
experimental_model
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
limitations
Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested.
nutrient_topic
Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
organism
Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol
plain_language
Indicaxanthin prevented 7-ketocholesterol-associated NOX4 overexpression in THP-1 cells.
primary_references
Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
route
In vitro co-incubation
tissue
Myeloid cells; cytosol and mitochondria
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 327–335
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol · source_derived_draft · unverified_draft
## betalains-thp1-nox4 Indicaxanthin prevented 7-ketocholesterol-associated NOX4 overexpression in THP-1 cells. Model/species: Human THP-1 monocyte/macrophage cells challenged with 7-ketocholesterol Tissue: Myeloid cells; cytosol and mitochondria Exposure: Indicaxanthin 2.5 micromolar; 7-ketocholesterol challenge concentration not specified in accessed abstract Route: In vitro co-incubation Duration: Kinetic observations within 24 h Limits: Calcium preservation is not calcium chelation, dietary calcium depletion or proof of a specific calcium-channel target; clinical plaque regression was not tested. Primary reference: Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress. (2013). https://pubmed.ncbi.nlm.nih.gov/23228674/ DOI: 10.1017/S000711451200493X
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.

DPI blocks the indicaxanthin-associated macrophage PGD2 response

Condition: machinery_impairment · DPI co-incubation at 1 micromolar.

Normal role: In this stimulated-cell setting indicaxanthin promotes lipid hydroperoxide and PGD2 formation.

Recorded consequence: The indicaxanthin-associated increase in PGD2 is prevented.

Scope: Pharmacological redox-enzyme perturbation at high cell-culture indicaxanthin exposure.

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.

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20)Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · unverified_draftRead preserved source
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20)Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. 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.

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

Indicaxanthin

The mechanisms

Added indicaxanthin increased resistance of beta-thalassemic red cells to peroxide-induced haemolysis.

Added indicaxanthin delayed vitamin E depletion during oxidative challenge of beta-thalassemic red cells.

Added indicaxanthin delayed glutathione depletion during oxidative challenge of beta-thalassemic red cells.

Indicaxanthin reduced the perferryl-haemoglobin intermediate in the spectrophotometric reaction system.

Indicaxanthin showed absorptive apparent permeability of 4.4 +/- 0.4 x 10^-6 cm/s in the 2013 Caco-2 transport experiment.

Indicaxanthin transport was non-polarized and insensitive to the tested transporter inhibitors; EDTA treatment increased its passage.

Adding indicaxanthin reduced spontaneous contractile activity of isolated mouse ileal longitudinal muscle.

Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle.

Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity.

Indicaxanthin pretreatment reduced LPS-induced microsomal PGE synthase-1 overexpression in RAW 264.7 cells.

Indicaxanthin pretreatment increased COX-2 expression in LPS-stimulated RAW 264.7 cells.

Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells.

Indicaxanthin pretreatment increased production of 15-deoxy-PGJ2 in LPS-stimulated RAW 264.7 cells.

Indicaxanthin increased early lipid hydroperoxide accumulation above the LPS-only level in RAW 264.7 cells.

Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages.

Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages.

After oral indicaxanthin, rat whole-brain content peaked at 20 +/- 2.4 ng at 2.5 hours.

Local indicaxanthin application reduced spontaneous firing of rat hippocampal neurons in a dose-related manner.

Local indicaxanthin at 0.34 ng/neuron reduced glutamate-evoked excitation in rat hippocampal recordings.

After oral indicaxanthin, pigment was detected in rat cortex, hippocampus, diencephalon, brainstem and cerebellum, but not the striato-pallidal complex.

Local indicaxanthin reduced cortical-neuron firing at the two higher tested amounts in rats.

Local indicaxanthin increased firing in rat striatal neurons, contrasting with its predominant inhibitory response in other recorded regions.

Yellow-cactus-pear consumption was associated with increased motor-cortex intracortical facilitation in the preliminary human study.

The six-person imaging subgroup showed no significant resting-state connectivity change after the fruit meal.

Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone.

Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells.

Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells.

Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment.

N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells.

Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs.

Indicaxanthin pretreatment prevented the oxidized-LDL-associated decrease in ABCA1 mRNA and protein in HUVECs.

Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 mRNA and protein increases in HUVECs.

Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs.

Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells.

Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells.

Purified indicaxanthin inhibited proliferating Caco-2-cell growth, with a reported IC50 of 115 +/- 15 micromolar.

Indicaxanthin treatment increased the LC3-II marker in Caco-2 cells.

Indicaxanthin at 50 micromolar increased Beclin1 protein abundance in Caco-2 cells.

Indicaxanthin at 50 or 100 micromolar increased acidic-vesicle fluorescence in Caco-2 cells.

Indicaxanthin treatment shifted the Caco-2 RRBS profile toward greater genomic CpG methylation, most strongly at 50 micromolar.

The 2025 Caco-2 methylome analysis associated indicaxanthin exposure with increased methylation at rDNA loci.

Oral indicaxanthin reduced cortical TUNEL-positive cells in high-fat-diet-fed male mice.

Oral indicaxanthin altered gut microbial relative abundances in high-fat-diet-fed male mice.

Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta.

Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells.

Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.

Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells.

Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.

Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.

Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols.

LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.

Indicaxanthin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed.

Indicaxanthin reacted directly with hypochlorous acid in the kinetic assay.

After cactus pear ingestion, plasma indicaxanthin peaked at 3 h and was undetectable by 12 h.

Adding indicaxanthin to human plasma produced pigment-enriched LDL after particle isolation.

LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation.

Indicaxanthin lowered NOX2 mRNA in the stimulated murine macrophage comparison.

Indicaxanthin increased ROS beyond the hydrogen-peroxide-challenged level in RAW 264.7 cells.

Indicaxanthin donated one electron to MPO compound I, producing compound II.

Indicaxanthin reduced MPO compound II to the native ferric enzyme.

Indicaxanthin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s.

Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action.

Indicaxanthin reduced ATP depletion during smoke-extract exposure of isolated red cells.

Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells.

Indicaxanthin prevented smoke-extract-triggered Fas aggregation and recruitment of FADD and caspase-8 at erythrocyte membranes.

Indicaxanthin reduced smoke-extract-induced phosphatidylserine externalization.

Co-incubating 2.5 micromolar indicaxanthin prevented the measured 7-ketocholesterol-induced pro-apoptotic events.

Indicaxanthin preserved cytosolic calcium homeostasis during the 7-ketocholesterol challenge.

Indicaxanthin prevented 7-ketocholesterol-associated NOX4 overexpression in THP-1 cells.

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