Luteolin / 3′,4′,5,7-tetrahydroxyflavone

evidence_access

Primary abstract

experimental_model

Human CD38 enzyme assay with docking.

limitations

Docking does not prove a binding pose; no human NAD increase or longevity effect established.

nutrient_topic

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

plain_language

One experimentally inhibited target consumes NAD-related substrates.

primary_references

Flavonoids as inhibitors of human CD38. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21641214/ · DOI 10.1016/j.bmcl.2011.05.022

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CD38 enzyme assay with docking. · source_derived_draft · unverified_draft

## luteolin-cd38-inhibition One experimentally inhibited target consumes NAD-related substrates. Luteolin inhibited human CD38 at an IC50 below 10 micromolar in vitro. Model: Human CD38 enzyme assay with docking. Limitations: Docking does not prove a binding pose; no human NAD increase or longevity effect established. Evidence access: Primary abstract Flavonoids as inhibitors of human CD38. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21641214/ · DOI 10.1016/j.bmcl.2011.05.022

evidence_access

Primary abstract

experimental_model

Recombinant human alpha-prime plus beta; radiolabeled ATP transfer.

limitations

Assay potency is not an oral therapeutic concentration.

nutrient_topic

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

plain_language

A measured kinase effect uses a defined human subunit combination.

primary_references

Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19197122/

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human alpha-prime plus beta; radiolabeled ATP transfer. · source_derived_draft · unverified_draft

## luteolin-ck2-human A measured kinase effect uses a defined human subunit combination. Luteolin inhibited reconstituted human CK2 alpha-prime/beta holoenzyme, IC50 0.86 micromolar. Model: Recombinant human alpha-prime plus beta; radiolabeled ATP transfer. Limitations: Assay potency is not an oral therapeutic concentration. Evidence access: Primary abstract Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19197122/

evidence_access

Primary abstract

experimental_model

CK2 inhibitor kinetics and maize catalytic-subunit crystal structure.

limitations

Do not relabel the crystal as human CK2.

nutrient_topic

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

plain_language

The structural experiment used a plant enzyme.

primary_references

Inhibition of protein kinase CK2 by flavonoids and tyrphostins. A structural insight. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22794353/ · DOI 10.1021/bi300531c

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CK2 inhibitor kinetics and maize catalytic-subunit crystal structure. · source_derived_draft · unverified_draft

## luteolin-ck2-plant-structure The structural experiment used a plant enzyme. Crystallography located luteolin in the catalytic pocket of Zea mays CK2; kinase inhibition was ATP-competitive. Model: CK2 inhibitor kinetics and maize catalytic-subunit crystal structure. Limitations: Do not relabel the crystal as human CK2. Evidence access: Primary abstract Inhibition of protein kinase CK2 by flavonoids and tyrphostins. A structural insight. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22794353/ · DOI 10.1021/bi300531c

evidence_access

Primary abstract

experimental_model

Cell-free Cu(II) spectroscopy.

limitations

Metal, pH and preparation matter; no human copper-balance measurement.

nutrient_topic

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

plain_language

Copper need not bind at the same site assigned for iron.

primary_references

The effect of Luteolin on DNA damage mediated by a copper catalyzed Fenton reaction. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34717250/ · DOI 10.1016/j.jinorgbio.2021.111635

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free Cu(II) spectroscopy. · source_derived_draft · unverified_draft

## luteolin-copper-binding Copper need not bind at the same site assigned for iron. Spectroscopy assigned Cu(II) coordination by luteolin to the 5-hydroxyl/4-carbonyl region. Model: Cell-free Cu(II) spectroscopy. Limitations: Metal, pH and preparation matter; no human copper-balance measurement. Evidence access: Primary abstract The effect of Luteolin on DNA damage mediated by a copper catalyzed Fenton reaction. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34717250/ · DOI 10.1016/j.jinorgbio.2021.111635

evidence_access

Primary abstract

experimental_model

EPR spin trapping and DNA gel electrophoresis.

limitations

Neither cancer prevention nor clinical copper depletion follows from this assay.

nutrient_topic

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

plain_language

This chemical assay showed protection rather than inevitable metal-driven damage.

primary_references

The effect of Luteolin on DNA damage mediated by a copper catalyzed Fenton reaction. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34717250/ · DOI 10.1016/j.jinorgbio.2021.111635

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · EPR spin trapping and DNA gel electrophoresis. · source_derived_draft · unverified_draft

## luteolin-copper-fenton This chemical assay showed protection rather than inevitable metal-driven damage. Luteolin–copper coordination suppressed radical formation and luteolin dose-dependently protected DNA in the Cu-Fenton assay. Model: EPR spin trapping and DNA gel electrophoresis. Limitations: Neither cancer prevention nor clinical copper depletion follows from this assay. Evidence access: Primary abstract The effect of Luteolin on DNA damage mediated by a copper catalyzed Fenton reaction. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34717250/ · DOI 10.1016/j.jinorgbio.2021.111635

evidence_access

Primary full text

experimental_model

Human GPVI binding assays.

limitations

Binding-site mutations and crystal confirmation were not provided.

nutrient_topic

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

plain_language

A platelet collagen receptor is a measured binding target.

primary_references

Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human GPVI binding assays. · source_derived_draft · unverified_draft

## luteolin-gpvi-binding A platelet collagen receptor is a measured binding target. SPR supported luteolin binding to human GPVI, and a solid-phase assay showed reduced collagen–GPVI interaction. Model: Human GPVI binding assays. Limitations: Binding-site mutations and crystal confirmation were not provided. Evidence access: Primary full text Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

evidence_access

Primary abstract

experimental_model

Human cultured cancer cells.

limitations

Readout does not prove direct binding to each enzyme or identify one causal isoform.

nutrient_topic

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

plain_language

Several regulators changed together.

primary_references

The dietary flavone luteolin epigenetically activates the Nrf2 pathway and blocks cell transformation in human colorectal cancer HCT116 cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30129150/ · DOI 10.1002/jcb.27275

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cultured cancer cells. · source_derived_draft · unverified_draft

## luteolin-human-epigenetic-enzymes Several regulators changed together. Luteolin reduced measured DNMT and HDAC protein levels and activities in HCT116 cells. Model: Human cultured cancer cells. Limitations: Readout does not prove direct binding to each enzyme or identify one causal isoform. Evidence access: Primary abstract The dietary flavone luteolin epigenetically activates the Nrf2 pathway and blocks cell transformation in human colorectal cancer HCT116 cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30129150/ · DOI 10.1002/jcb.27275

evidence_access

Primary abstract

experimental_model

Human colorectal cell culture and bisulfite sequencing.

limitations

Different model; not a proven contradiction or universal epigenetic reset.

nutrient_topic

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

plain_language

The direction differs from the mouse-liver result.

primary_references

The dietary flavone luteolin epigenetically activates the Nrf2 pathway and blocks cell transformation in human colorectal cancer HCT116 cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30129150/ · DOI 10.1002/jcb.27275

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colorectal cell culture and bisulfite sequencing. · source_derived_draft · unverified_draft

## luteolin-human-nrf2-up The direction differs from the mouse-liver result. Luteolin reduced NFE2L2-promoter methylation and increased Nrf2 expression in human HCT116 colorectal cells. Model: Human colorectal cell culture and bisulfite sequencing. Limitations: Different model; not a proven contradiction or universal epigenetic reset. Evidence access: Primary abstract The dietary flavone luteolin epigenetically activates the Nrf2 pathway and blocks cell transformation in human colorectal cancer HCT116 cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30129150/ · DOI 10.1002/jcb.27275

evidence_access

Primary abstract

experimental_model

Human oral exposure; primary abstract does not specify dose.

limitations

Does not establish free intracellular luteolin or clinical target engagement.

nutrient_topic

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

plain_language

The swallowed molecule and the main measured blood form differ.

primary_references

Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human oral exposure; primary abstract does not specify dose. · source_derived_draft · unverified_draft

## luteolin-human-sulfate The swallowed molecule and the main measured blood form differ. After oral luteolin aglycone in human volunteers, luteolin 3′-O-sulfate was the principal plasma form identified. Model: Human oral exposure; primary abstract does not specify dose. Limitations: Does not establish free intracellular luteolin or clinical target engagement. Evidence access: Primary abstract Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273

evidence_access

Primary abstract

experimental_model

Spectroscopy, mass spectrometry and electrochemistry.

limitations

Solvent-specific chemistry does not establish intestinal iron depletion.

nutrient_topic

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

plain_language

Iron binding depends on chemical conditions.

primary_references

Spectroscopic and electrochemical studies on the evaluation of the radical scavenging activities of luteolin by chelating iron · 2014 · https://pubs.rsc.org/en/content/articlelanding/2014/ra/c4ra01396d · DOI 10.1039/C4RA01396D

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Spectroscopy, mass spectrometry and electrochemistry. · source_derived_draft · unverified_draft

## luteolin-iron-binding Iron binding depends on chemical conditions. Luteolin formed a 1:1 Fe(III) complex in ethanol, with the B-ring catechol assigned as the binding site. Model: Spectroscopy, mass spectrometry and electrochemistry. Limitations: Solvent-specific chemistry does not establish intestinal iron depletion. Evidence access: Primary abstract Spectroscopic and electrochemical studies on the evaluation of the radical scavenging activities of luteolin by chelating iron · 2014 · https://pubs.rsc.org/en/content/articlelanding/2014/ra/c4ra01396d · DOI 10.1039/C4RA01396D

evidence_access

Primary abstract

experimental_model

Cell-free chemical system.

limitations

Not a human nutrient requirement or treatment for iron overload.

nutrient_topic

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

plain_language

Metal binding and radical chemistry can act together.

primary_references

Spectroscopic and electrochemical studies on the evaluation of the radical scavenging activities of luteolin by chelating iron · 2014 · https://pubs.rsc.org/en/content/articlelanding/2014/ra/c4ra01396d · DOI 10.1039/C4RA01396D

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free chemical system. · source_derived_draft · unverified_draft

## luteolin-iron-fenton Metal binding and radical chemistry can act together. Luteolin suppressed Fenton radical generation through combined Fe(II) chelation and radical scavenging. Model: Cell-free chemical system. Limitations: Not a human nutrient requirement or treatment for iron overload. Evidence access: Primary abstract Spectroscopic and electrochemical studies on the evaluation of the radical scavenging activities of luteolin by chelating iron · 2014 · https://pubs.rsc.org/en/content/articlelanding/2014/ra/c4ra01396d · DOI 10.1039/C4RA01396D

evidence_access

Primary abstract

experimental_model

Human mast-cell cultures; 1–100 micromolar pretreatment.

limitations

Do not assign the analog’s animal or calcium results to luteolin.

nutrient_topic

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

plain_language

Related flavones have different potencies.

primary_references

The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human mast-cell cultures; 1–100 micromolar pretreatment. · source_derived_draft · unverified_draft

## luteolin-mast-histamine Related flavones have different potencies. Luteolin reduced stimulated histamine release from human LAD2 mast cells; tetramethoxyluteolin was more potent. Model: Human mast-cell cultures; 1–100 micromolar pretreatment. Limitations: Do not assign the analog’s animal or calcium results to luteolin. Evidence access: Primary abstract The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

evidence_access

Primary abstract

experimental_model

Substance-P or IgE/anti-IgE mast-cell experiments.

limitations

Not a clinical comparison of oral treatments.

nutrient_topic

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

plain_language

It affected another mediator besides histamine.

primary_references

The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Substance-P or IgE/anti-IgE mast-cell experiments. · source_derived_draft · unverified_draft

## luteolin-mast-tnf It affected another mediator besides histamine. Luteolin inhibited preformed TNF secretion from activated human LAD2 mast cells. Model: Substance-P or IgE/anti-IgE mast-cell experiments. Limitations: Not a clinical comparison of oral treatments. Evidence access: Primary abstract The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

evidence_access

Primary abstract

experimental_model

Mouse BV-2 and primary-microglia experiments.

limitations

Pathway readouts do not prove direct JNK binding.

nutrient_topic

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

plain_language

One inflammatory signaling route was suppressed.

primary_references

Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse BV-2 and primary-microglia experiments. · source_derived_draft · unverified_draft

## luteolin-microglia-ap1 One inflammatory signaling route was suppressed. Luteolin reduced AP-1 DNA binding and JNK phosphorylation in LPS-stimulated mouse BV-2 microglia. Model: Mouse BV-2 and primary-microglia experiments. Limitations: Pathway readouts do not prove direct JNK binding. Evidence access: Primary abstract Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

evidence_access

Primary abstract

experimental_model

Mouse cells and 21-day drinking-water pretreatment.

limitations

Animal exposure does not establish a human neuroprotective dose.

nutrient_topic

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

plain_language

The response differed by brain region.

primary_references

Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse cells and 21-day drinking-water pretreatment. · source_derived_draft · unverified_draft

## luteolin-microglia-il6 The response differed by brain region. Luteolin reduced LPS-induced IL-6 expression in mouse microglia and hippocampus; cortex and cerebellum did not show the same reduction. Model: Mouse cells and 21-day drinking-water pretreatment. Limitations: Animal exposure does not establish a human neuroprotective dose. Evidence access: Primary abstract Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

evidence_access

Primary abstract

experimental_model

Mouse BV-2 cells with LPS.

limitations

Different stimuli or timings can yield different responses.

nutrient_topic

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

plain_language

Anti-inflammatory activity need not mean every pathway is blocked.

primary_references

Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse BV-2 cells with LPS. · source_derived_draft · unverified_draft

## luteolin-microglia-nfkb-null Anti-inflammatory activity need not mean every pathway is blocked. Luteolin did not reduce LPS-induced NF-kappaB DNA binding or I-kappaB-alpha degradation in this microglial experiment. Model: Mouse BV-2 cells with LPS. Limitations: Different stimuli or timings can yield different responses. Evidence access: Primary abstract Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18490655/ · DOI 10.1073/pnas.0802865105

evidence_access

Primary abstract

experimental_model

Mouse liver dosing study.

limitations

Not evidence of universal human glutathione depletion.

nutrient_topic

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

plain_language

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

primary_references

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

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

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

evidence_access

Primary full text

experimental_model

Washed human platelets, 2.5–25 micromolar range in activation assays.

limitations

Not systemic calcium depletion or evidence of human bleeding safety.

nutrient_topic

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

plain_language

Calcium signaling connects receptor activation to platelet release.

primary_references

Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Washed human platelets, 2.5–25 micromolar range in activation assays. · source_derived_draft · unverified_draft

## luteolin-platelet-calcium Calcium signaling connects receptor activation to platelet release. Luteolin reduced collagen/convulxin-induced calcium responses and secretion in washed human platelets. Model: Washed human platelets, 2.5–25 micromolar range in activation assays. Limitations: Not systemic calcium depletion or evidence of human bleeding safety. Evidence access: Primary full text Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

evidence_access

Primary full text

experimental_model

Washed human platelets; 10-minute pretreatment.

limitations

Higher concentrations and longer incubation can differ.

nutrient_topic

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

plain_language

A negative result limits the idea of universal platelet blockade.

primary_references

Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Washed human platelets; 10-minute pretreatment. · source_derived_draft · unverified_draft

## luteolin-platelet-stimulus A negative result limits the idea of universal platelet blockade. At 25 micromolar, luteolin did not significantly inhibit ADP- or U46619-induced aggregation in the short-incubation protocol. Model: Washed human platelets; 10-minute pretreatment. Limitations: Higher concentrations and longer incubation can differ. Evidence access: Primary full text Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/38026984/ · DOI 10.3389/fphar.2023.1255069

evidence_access

Primary abstract

experimental_model

Mouse adipocyte differentiation and gene expression.

limitations

GLUT4 expression is not proof of increased glucose uptake in humans.

nutrient_topic

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

plain_language

One receptor can produce different responses at different genes.

primary_references

Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

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

## luteolin-pparg-gene-specific One receptor can produce different responses at different genes. In mouse 3T3-L1 cells, luteolin suppressed adipogenesis and several PPAR gamma targets while increasing GLUT4 expression. Model: Mouse adipocyte differentiation and gene expression. Limitations: GLUT4 expression is not proof of increased glucose uptake in humans. Evidence access: Primary abstract Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

evidence_access

Primary abstract

experimental_model

PPAR gamma ligand-binding-domain crystallography.

limitations

Simulated cooperative stabilization is not demonstrated nutritional synergy.

nutrient_topic

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

plain_language

Two ligands fit in the structural preparation.

primary_references

Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · PPAR gamma ligand-binding-domain crystallography. · source_derived_draft · unverified_draft

## luteolin-pparg-ligand Two ligands fit in the structural preparation. Luteolin occupied the PPAR gamma ligand pocket in an inactive conformer; myristic acid simultaneously occupied the pocket. Model: PPAR gamma ligand-binding-domain crystallography. Limitations: Simulated cooperative stabilization is not demonstrated nutritional synergy. Evidence access: Primary abstract Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

availability_state

biomarker_context Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Rat intravenous LPS experiment.

limitations

Association supports deconjugation; not a universal human targeting mechanism.

nutrient_topic

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

plain_language

Inflammatory state altered measured forms.

primary_references

Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/

trigger_kind

biomarker_context Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 164–170

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat intravenous LPS experiment. · source_derived_draft · unverified_draft

## luteolin-rat-deconjugation Inflammatory state altered measured forms. LPS-treated rats showed increased plasma beta-glucuronidase activity and a higher free-luteolin/monoglucuronide ratio. Model: Rat intravenous LPS experiment. Limitations: Association supports deconjugation; not a universal human targeting mechanism. Evidence access: Primary abstract Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/

evidence_access

Primary abstract

experimental_model

Rat oral aglycone and green-pepper-leaf glucosides.

limitations

Species and administered form affect exposure. The glucuronide pool is not a single positional isomer.

nutrient_topic

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

plain_language

Rat metabolism cannot be copied directly onto humans.

primary_references

Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 20–26

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat oral aglycone and green-pepper-leaf glucosides. · source_derived_draft · unverified_draft

## luteolin-rat-glucuronides Rat metabolism cannot be copied directly onto humans. Rats given luteolin aglycone or the tested glucosides predominantly contained glucuronides in plasma and organs. Model: Rat oral aglycone and green-pepper-leaf glucosides. Limitations: Species and administered form affect exposure. The glucuronide pool is not a single positional isomer. Evidence access: Primary abstract Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273

evidence_access

Primary full text

experimental_model

HepG2 culture, 3.5 mM CCl4.

limitations

Not direct binding, transporter flux, or normal human-liver exposure.

nutrient_topic

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

plain_language

Cystine-handling machinery responded in an injury model.

primary_references

Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38755566/ · DOI 10.1186/s12906-024-04486-2

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · HepG2 culture, 3.5 mM CCl4. · source_derived_draft · unverified_draft

## luteolin-slc7a11-expression Cystine-handling machinery responded in an injury model. At 5 micromolar, luteolin increased SLC7A11 expression in CCl4-challenged human HepG2 cells. Model: HepG2 culture, 3.5 mM CCl4. Limitations: Not direct binding, transporter flux, or normal human-liver exposure. Evidence access: Primary full text Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38755566/ · DOI 10.1186/s12906-024-04486-2

evidence_access

Primary full text

experimental_model

Human cell ChIP; 10–60 micromolar studies.

limitations

Promoter association is not a direct luteolin–TET1 binding assay.

nutrient_topic

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

plain_language

DNA-modifying machinery participates in the response.

primary_references

Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cell ChIP; 10–60 micromolar studies. · source_derived_draft · unverified_draft

## luteolin-tet1-recruitment DNA-modifying machinery participates in the response. Luteolin increased TET1 association with the NFE2L2 promoter in human colon cancer cells. Model: Human cell ChIP; 10–60 micromolar studies. Limitations: Promoter association is not a direct luteolin–TET1 binding assay. Evidence access: Primary full text Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y

evidence_access

Primary abstract

experimental_model

Volunteers receiving a luteolin-containing formulation.

limitations

Different measurement levels, not an unresolved contradiction.

nutrient_topic

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

plain_language

A urine ratio reflects formation plus subsequent clearance.

primary_references

Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Volunteers receiving a luteolin-containing formulation. · source_derived_draft · unverified_draft

## luteolin-urinary-methyl-bias A urine ratio reflects formation plus subsequent clearance. Human urine favored the 3′-methylated product despite the opposite initial COMT preference. Model: Volunteers receiving a luteolin-containing formulation. Limitations: Different measurement levels, not an unresolved contradiction. Evidence access: Primary abstract Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

evidence_access

Primary full text

experimental_model

Recombinant kinase and human HeLa-cell experiments.

limitations

Not a selective VRK1 inhibitor or a demonstrated cancer therapy.

nutrient_topic

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

plain_language

Kinase inhibition changed a nuclear-envelope regulator.

primary_references

Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25310002/ · DOI 10.1371/journal.pone.0109655

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant kinase and human HeLa-cell experiments. · source_derived_draft · unverified_draft

## luteolin-vrk1-baf Kinase inhibition changed a nuclear-envelope regulator. Luteolin reduced VRK1-mediated BAF phosphorylation; 10 micromolar treatment altered nuclear morphology in HeLa cells. Model: Recombinant kinase and human HeLa-cell experiments. Limitations: Not a selective VRK1 inhibitor or a demonstrated cancer therapy. Evidence access: Primary full text Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25310002/ · DOI 10.1371/journal.pone.0109655

evidence_access

Primary full text

experimental_model

Recombinant protein and human-cell lysates.

limitations

No crystal-defined pose; published SPR table constants are not used here as a validated affinity.

nutrient_topic

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

plain_language

Physical binding evidence accompanies the kinase result.

primary_references

Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25310002/ · DOI 10.1371/journal.pone.0109655

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 348–354

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant protein and human-cell lysates. · source_derived_draft · unverified_draft

## luteolin-vrk1-binding Physical binding evidence accompanies the kinase result. Pull-down, SPR and NMR experiments supported direct luteolin binding near the human VRK1 catalytic domain. Model: Recombinant protein and human-cell lysates. Limitations: No crystal-defined pose; published SPR table constants are not used here as a validated affinity. Evidence access: Primary full text Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25310002/ · DOI 10.1371/journal.pone.0109655

evidence_access

Primary abstract

experimental_model

Purified bovine enzyme steady-state kinetics.

limitations

Bovine enzyme evidence; not a clinical urate-lowering trial.

nutrient_topic

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

plain_language

It interfered with the purine-breakdown enzyme.

primary_references

Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine enzyme steady-state kinetics. · source_derived_draft · unverified_draft

## luteolin-xo-inhibition It interfered with the purine-breakdown enzyme. Luteolin competitively inhibited purified bovine xanthine oxidase without time-dependent inhibition. Model: Purified bovine enzyme steady-state kinetics. Limitations: Bovine enzyme evidence; not a clinical urate-lowering trial. Evidence access: Primary abstract Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123

evidence_access

Primary abstract

experimental_model

Bovine enzyme assays.

limitations

Does not establish antioxidant benefit across tissues.

nutrient_topic

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

plain_language

Blocking the enzyme also reduced its radical output.

primary_references

Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 292–298

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Bovine enzyme assays. · source_derived_draft · unverified_draft

## luteolin-xo-superoxide Blocking the enzyme also reduced its radical output. Luteolin reduced superoxide production by purified bovine xanthine oxidase. Model: Bovine enzyme assays. Limitations: Does not establish antioxidant benefit across tissues. Evidence access: Primary abstract Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123

evidence_access

Primary abstract

experimental_model

Human CYP expression and liver microsomes.

limitations

Not evidence that the two oral products give equivalent exposures.

nutrient_topic

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

plain_language

A related flavone can be converted into luteolin.

primary_references

In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP expression and liver microsomes. · source_derived_draft · unverified_draft

## luteolin-cyp1a2-apigenin A related flavone can be converted into luteolin. Recombinant human CYP1A2 supported apigenin 3′-hydroxylation to luteolin. Model: Human CYP expression and liver microsomes. Limitations: Not evidence that the two oral products give equivalent exposures. Evidence access: Primary abstract In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9

evidence_access

Primary abstract

experimental_model

Human CYP expression and liver microsomes.

limitations

Not evidence that the two oral products give equivalent exposures.

nutrient_topic

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

plain_language

A related flavone can be converted into luteolin.

primary_references

In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP expression and liver microsomes. · source_derived_draft · unverified_draft

## luteolin-cyp3a4-apigenin A related flavone can be converted into luteolin. Recombinant human CYP3A4 supported apigenin 3′-hydroxylation to luteolin. Model: Human CYP expression and liver microsomes. Limitations: Not evidence that the two oral products give equivalent exposures. Evidence access: Primary abstract In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9

evidence_access

Primary abstract

experimental_model

Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC.

limitations

Position of the monoglucuronide is not resolved in the abstract.

nutrient_topic

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

plain_language

Inflamed cells can locally regenerate the unconjugated molecule.

primary_references

Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 156–162

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC. · source_derived_draft · unverified_draft

## luteolin-neutrophil-release Inflamed cells can locally regenerate the unconjugated molecule. Supernatants from activated human neutrophils converted luteolin monoglucuronide to free luteolin, consistent with released beta-glucuronidase. Model: Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC. Limitations: Position of the monoglucuronide is not resolved in the abstract. Evidence access: Primary abstract Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Rat intravenous luteolin with COMT inhibition.

limitations

Not a measured human oral drug interaction.

nutrient_topic

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

plain_language

Blocking one metabolic exit increased parent exposure.

primary_references

Role of catechol-O-methyltransferase in the disposition of luteolin in rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21209248/ · DOI 10.1124/dmd.110.037333

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 132–138

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat intravenous luteolin with COMT inhibition. · source_derived_draft · unverified_draft

## luteolin-rat-comt-blockade Blocking one metabolic exit increased parent exposure. Entacapone coadministration reduced methylated luteolin products and increased circulating luteolin in rats. Model: Rat intravenous luteolin with COMT inhibition. Limitations: Not a measured human oral drug interaction. Evidence access: Primary abstract Role of catechol-O-methyltransferase in the disposition of luteolin in rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21209248/ · DOI 10.1124/dmd.110.037333

evidence_access

Primary abstract

experimental_model

Human recombinant UGT comparison and microsomes.

limitations

Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.

nutrient_topic

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

plain_language

A specific enzyme can attach a glucuronide group.

primary_references

Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 28–34

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft

## luteolin-ugt1a1-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A1 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

evidence_access

Primary abstract

experimental_model

Human recombinant UGT comparison and microsomes.

limitations

Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.

nutrient_topic

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

plain_language

A specific enzyme can attach a glucuronide group.

primary_references

Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft

## luteolin-ugt1a8-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A8 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

evidence_access

Primary abstract

experimental_model

Human recombinant UGT comparison and microsomes.

limitations

Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.

nutrient_topic

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

plain_language

A specific enzyme can attach a glucuronide group.

primary_references

Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft

## luteolin-ugt1a9-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A9 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705

evidence_access

Primary abstract

experimental_model

20 mM glucose for 48 hours with osmotic and normoglycemic controls.

limitations

Combination activity is not demonstrated clinical synergy; assess interaction statistics before claiming more-than-additive benefit.

nutrient_topic

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

plain_language

Two compounds were actually tested together.

primary_references

Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 440–446

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 20 mM glucose for 48 hours with osmotic and normoglycemic controls. · source_derived_draft · unverified_draft

## fisetin-luteolin-combination Two compounds were actually tested together. In high-glucose-treated human THP-1 cells, 500 nM fisetin plus 500 nM or 1 micromolar luteolin suppressed inflammatory output. Model: 20 mM glucose for 48 hours with osmotic and normoglycemic controls. Limitations: Combination activity is not demonstrated clinical synergy; assess interaction statistics before claiming more-than-additive benefit. Evidence access: Primary abstract Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

UGT1A9-expressing human HeLa cells.

limitations

Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients.

nutrient_topic

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

plain_language

Blocking export changes where metabolites accumulate.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 84–90

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · UGT1A9-expressing human HeLa cells. · source_derived_draft · unverified_draft

## luteolin-abcg2-blockade Blocking export changes where metabolites accumulate. Ko143 inhibition of ABCG2 reduced luteolin-monoglucuronide efflux and increased intracellular retention. Model: UGT1A9-expressing human HeLa cells. Limitations: Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_access

Primary abstract

experimental_model

Human serum-albumin binding assay.

limitations

Binding alone does not establish displacement toxicity.

nutrient_topic

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

plain_language

Conjugation changes carrier binding.

primary_references

Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human serum-albumin binding assay. · source_derived_draft · unverified_draft

## luteolin-albumin-sulfate Conjugation changes carrier binding. Luteolin sulfate formed a more stable albumin complex than parent luteolin. Model: Human serum-albumin binding assay. Limitations: Binding alone does not establish displacement toxicity. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

evidence_access

Primary abstract

experimental_model

Human enzyme and liver-S9 kinetics.

limitations

Product formation is not identical to accumulation after further metabolism.

nutrient_topic

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

plain_language

The enzyme initially favored the diosmetin branch.

primary_references

Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme and liver-S9 kinetics. · source_derived_draft · unverified_draft

## luteolin-comt-para The enzyme initially favored the diosmetin branch. Human recombinant COMT and liver S9 favored 4′- over 3′-O-methylation of luteolin. Model: Human enzyme and liver-S9 kinetics. Limitations: Product formation is not identical to accumulation after further metabolism. Evidence access: Primary abstract Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

evidence_access

Primary abstract

experimental_model

Human CYP assays.

limitations

Restricted enzyme panel; not a blanket absence of interactions.

nutrient_topic

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

plain_language

The parent’s effects cannot simply be assigned to every metabolite.

primary_references

Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 244–250

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP assays. · source_derived_draft · unverified_draft

## luteolin-conjugate-cyp The parent’s effects cannot simply be assigned to every metabolite. Tested luteolin conjugates had no or weak inhibition of CYP2C9, CYP2C19 and CYP3A4. Model: Human CYP assays. Limitations: Restricted enzyme panel; not a blanket absence of interactions. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

evidence_access

Primary abstract

experimental_model

Recombinant human CYP comparison.

limitations

Explains a candidate source of urinary bias; not proof of drug induction.

nutrient_topic

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

plain_language

Downstream removal can reverse the apparent product preference.

primary_references

Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 100–106

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human CYP comparison. · source_derived_draft · unverified_draft

## luteolin-cyp1a2-demethylation Downstream removal can reverse the apparent product preference. Human CYP1A2 demethylated diosmetin more readily than chrysoeriol in vitro. Model: Recombinant human CYP comparison. Limitations: Explains a candidate source of urinary bias; not proof of drug induction. Evidence access: Primary abstract Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

evidence_access

Primary abstract

experimental_model

Recombinant human CYP comparison.

limitations

Explains a candidate source of urinary bias; not proof of drug induction.

nutrient_topic

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

plain_language

Downstream removal can reverse the apparent product preference.

primary_references

Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 108–114

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human CYP comparison. · source_derived_draft · unverified_draft

## luteolin-cyp3a4-demethylation Downstream removal can reverse the apparent product preference. Human CYP3A4 demethylated diosmetin more readily than chrysoeriol in vitro. Model: Recombinant human CYP comparison. Limitations: Explains a candidate source of urinary bias; not proof of drug induction. Evidence access: Primary abstract Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

evidence_access

Primary abstract

experimental_model

Recombinant human CYP comparison.

limitations

Explains a candidate source of urinary bias; not proof of drug induction.

nutrient_topic

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

plain_language

Downstream removal can reverse the apparent product preference.

primary_references

Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 116–122

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human CYP comparison. · source_derived_draft · unverified_draft

## luteolin-cyp3a5-demethylation Downstream removal can reverse the apparent product preference. Human CYP3A5 demethylated diosmetin more readily than chrysoeriol in vitro. Model: Recombinant human CYP comparison. Limitations: Explains a candidate source of urinary bias; not proof of drug induction. Evidence access: Primary abstract Luteolin is a rare substrate of human catechol-O-methyltransferase favoring a para-methylation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23386290/ · DOI 10.1002/mnfr.201200584

evidence_access

Primary full text

experimental_model

Mouse macrophage culture.

limitations

Expression alone does not show human glutathione restoration.

nutrient_topic

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

plain_language

A conjugate can influence glutathione-synthesis machinery.

primary_references

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

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

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

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

evidence_access

Primary full text

experimental_model

Mouse macrophages, 5–50 micromolar pretreatment.

limitations

Reduced phosphorylation is not proof of direct kinase binding.

nutrient_topic

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

plain_language

A conjugate has its own experimentally observed activity.

primary_references

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

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 500–506

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages, 5–50 micromolar pretreatment. · source_derived_draft · unverified_draft

## luteolin-glucuronide-tak1 A conjugate has its own experimentally observed activity. Luteolin 7-O-glucuronide reduced TAK1-pathway activation in LPS-stimulated RAW264.7 macrophages. Model: Mouse macrophages, 5–50 micromolar pretreatment. Limitations: Reduced phosphorylation is not proof of direct kinase binding. Evidence access: Primary full text Anti-Inflammatory and Anti-Oxidative Effects of luteolin-7-O-glucuronide in LPS-Stimulated Murine Macrophages through TAK1 Inhibition and Nrf2 Activation. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32187984/ · DOI 10.3390/ijms21062007

evidence_access

Primary abstract

experimental_model

Anaerobic resting-cell fermentation.

limitations

Intervening chalcones were proposed but not detected; do not invent confirmed enzyme steps.

nutrient_topic

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

plain_language

A smaller phenolic acid emerges downstream.

primary_references

Degradation of quercetin and luteolin by Eubacterium ramulus. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11722907/ · DOI 10.1128/AEM.67.12.5558-5567.2001

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 260–266

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Anaerobic resting-cell fermentation. · source_derived_draft · unverified_draft

## luteolin-microbial-end-product A smaller phenolic acid emerges downstream. Luteolin degradation by E. ramulus wK1 yielded dihydrocaffeic acid. Model: Anaerobic resting-cell fermentation. Limitations: Intervening chalcones were proposed but not detected; do not invent confirmed enzyme steps. Evidence access: Primary abstract Degradation of quercetin and luteolin by Eubacterium ramulus. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11722907/ · DOI 10.1128/AEM.67.12.5558-5567.2001

evidence_access

Primary abstract

experimental_model

Resting bacterial cells, HPLC and mass spectrometry.

limitations

Human-derived strain, not a measured conversion fraction in a person.

nutrient_topic

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

plain_language

Gut bacteria can change the flavone scaffold.

primary_references

Degradation of quercetin and luteolin by Eubacterium ramulus. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11722907/ · DOI 10.1128/AEM.67.12.5558-5567.2001

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 252–258

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Resting bacterial cells, HPLC and mass spectrometry. · source_derived_draft · unverified_draft

## luteolin-microbial-first-step Gut bacteria can change the flavone scaffold. Anaerobic E. ramulus wK1 converted luteolin through an identified eriodictyol intermediate. Model: Resting bacterial cells, HPLC and mass spectrometry. Limitations: Human-derived strain, not a measured conversion fraction in a person. Evidence access: Primary abstract Degradation of quercetin and luteolin by Eubacterium ramulus. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11722907/ · DOI 10.1128/AEM.67.12.5558-5567.2001

evidence_access

Primary abstract

experimental_model

Bacterial substrate-degradation study.

limitations

Not evidence that all gut communities behave identically.

nutrient_topic

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

plain_language

Changing sugar position changed bacterial access.

primary_references

Anaerobic degradation of flavonoids by Eubacterium ramulus. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10648107/ · DOI 10.1007/s002030050010

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 268–274

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

## luteolin-microbial-glucoside-selectivity Changing sugar position changed bacterial access. E. ramulus degraded luteolin 7-glucoside but not luteolin 5-glucoside under the tested anaerobic conditions. Model: Bacterial substrate-degradation study. Limitations: Not evidence that all gut communities behave identically. Evidence access: Primary abstract Anaerobic degradation of flavonoids by Eubacterium ramulus. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10648107/ · DOI 10.1007/s002030050010

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Wild-type versus Nrf2-null mice.

limitations

Knockout context does not define a dietary deficiency.

nutrient_topic

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

plain_language

Removing the regulator changed the response to the compound.

primary_references

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

trigger_kind

machinery_impairment Imported condition classification; unverified.

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

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

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

evidence_access

Primary abstract

experimental_model

Human transporter interaction assays.

limitations

No clinical drug-exposure change was measured.

nutrient_topic

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

plain_language

A transported metabolite can also compete with uptake.

primary_references

Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 228–234

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human transporter interaction assays. · source_derived_draft · unverified_draft

## luteolin-oatp1b1-inhibition-glucuronide A transported metabolite can also compete with uptake. Luteolin 3′-O-glucuronide strongly inhibited OATP1B1 in vitro. Model: Human transporter interaction assays. Limitations: No clinical drug-exposure change was measured. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

evidence_access

Primary abstract

experimental_model

Human transporter interaction assays.

limitations

No clinical drug-exposure change was measured.

nutrient_topic

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

plain_language

A transported metabolite can also compete with uptake.

primary_references

Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 220–226

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human transporter interaction assays. · source_derived_draft · unverified_draft

## luteolin-oatp1b1-inhibition-sulfate A transported metabolite can also compete with uptake. Luteolin 3′-O-sulfate strongly inhibited OATP1B1 in vitro. Model: Human transporter interaction assays. Limitations: No clinical drug-exposure change was measured. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

evidence_access

Primary abstract

experimental_model

Human corneal epithelial cell culture.

limitations

Not an oral dry-eye treatment trial.

nutrient_topic

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

plain_language

An eye-surface model links inflammation and barrier function.

primary_references

Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 380–386

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

## luteolin-pparg-corneal An eye-surface model links inflammation and barrier function. Luteolin reduced IL-8 release and restored electrical resistance in hypertonic human corneal epithelial cultures through a PPAR gamma-dependent response. Model: Human corneal epithelial cell culture. Limitations: Not an oral dry-eye treatment trial. Evidence access: Primary abstract Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Human HepG2 loss/gain-of-function experiments.

limitations

Not a selective rescue test proving all luteolin effects require SLC7A11.

nutrient_topic

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

plain_language

Precursor handling and peroxide defense are linked.

primary_references

Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38755566/ · DOI 10.1186/s12906-024-04486-2

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 524–530

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human HepG2 loss/gain-of-function experiments. · source_derived_draft · unverified_draft

## luteolin-slc7a11-knockdown Precursor handling and peroxide defense are linked. SLC7A11 silencing lowered GPX4/FTMT expression and total glutathione while worsening ferroptosis-associated measurements in HepG2 cells. Model: Human HepG2 loss/gain-of-function experiments. Limitations: Not a selective rescue test proving all luteolin effects require SLC7A11. Evidence access: Primary full text Luteolin attenuates CCl4-induced hepatic injury by inhibiting ferroptosis via SLC7A11. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38755566/ · DOI 10.1186/s12906-024-04486-2

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 172–178

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco1b1-3g A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 3′-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 188–194

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco1b1-3s A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 3′-O-sulfate in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 180–186

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco1b1-7g A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 7-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the expressing cell Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 196–202

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco2b1-3g A circulating conjugate has a route into cells. Human SLCO2B1 transported Luteolin 3′-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the expressing cell Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 212–218

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco2b1-3s A circulating conjugate has a route into cells. Human SLCO2B1 transported Luteolin 3′-O-sulfate in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

evidence_access

Primary abstract

experimental_model

Living-cell uptake using 2-APB fluorescence enhancement.

limitations

Transport capacity is not clinical efficacy or net organ flux.

nutrient_topic

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

plain_language

A circulating conjugate has a route into cells.

primary_references

The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

transport_effect

raises Measured in a fluorescence-based uptake assay.

transport_pool

the expressing cell Measured in a fluorescence-based uptake assay.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 204–210

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

## luteolin-slco2b1-7g A circulating conjugate has a route into cells. Human SLCO2B1 transported Luteolin 7-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary full text

experimental_model

Human colon cancer siRNA experiment.

limitations

No clinical efficacy or nutrient-supplement rescue established.

nutrient_topic

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

plain_language

Removing machinery weakened the observed cell-death response.

primary_references

Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 492–498

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colon cancer siRNA experiment. · source_derived_draft · unverified_draft

## luteolin-tet1-knockdown Removing machinery weakened the observed cell-death response. TET1 knockdown reduced luteolin-associated sub-G1 accumulation and nuclear fragmentation. Model: Human colon cancer siRNA experiment. Limitations: No clinical efficacy or nutrient-supplement rescue established. Evidence access: Primary full text Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y

evidence_access

Primary abstract

experimental_model

Recombinant enzymes and UGT1A9-expressing HeLa cells.

limitations

Engineered expression; not a human organ concentration.

nutrient_topic

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

plain_language

The conjugation position defines a distinct product.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 76–82

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzymes and UGT1A9-expressing HeLa cells. · source_derived_draft · unverified_draft

## luteolin-ugt1a9-34g The conjugation position defines a distinct product. Human UGT1A9 formed Luteolin 3′,4′-diglucuronide in the luteolin-conjugation study. Model: Recombinant enzymes and UGT1A9-expressing HeLa cells. Limitations: Engineered expression; not a human organ concentration. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_access

Primary abstract

experimental_model

Recombinant enzymes and UGT1A9-expressing HeLa cells.

limitations

Engineered expression; not a human organ concentration.

nutrient_topic

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

plain_language

The conjugation position defines a distinct product.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 52–58

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzymes and UGT1A9-expressing HeLa cells. · source_derived_draft · unverified_draft

## luteolin-ugt1a9-3g The conjugation position defines a distinct product. Human UGT1A9 formed Luteolin 3′-O-glucuronide in the luteolin-conjugation study. Model: Recombinant enzymes and UGT1A9-expressing HeLa cells. Limitations: Engineered expression; not a human organ concentration. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_access

Primary abstract

experimental_model

Recombinant enzymes and UGT1A9-expressing HeLa cells.

limitations

Engineered expression; not a human organ concentration.

nutrient_topic

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

plain_language

The conjugation position defines a distinct product.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 60–66

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzymes and UGT1A9-expressing HeLa cells. · source_derived_draft · unverified_draft

## luteolin-ugt1a9-4g The conjugation position defines a distinct product. Human UGT1A9 formed Luteolin 4′-O-glucuronide in the luteolin-conjugation study. Model: Recombinant enzymes and UGT1A9-expressing HeLa cells. Limitations: Engineered expression; not a human organ concentration. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_access

Primary abstract

experimental_model

Recombinant enzymes and UGT1A9-expressing HeLa cells.

limitations

Engineered expression; not a human organ concentration.

nutrient_topic

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

plain_language

The conjugation position defines a distinct product.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 68–74

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzymes and UGT1A9-expressing HeLa cells. · source_derived_draft · unverified_draft

## luteolin-ugt1a9-7g The conjugation position defines a distinct product. Human UGT1A9 formed Luteolin 7-O-glucuronide in the luteolin-conjugation study. Model: Recombinant enzymes and UGT1A9-expressing HeLa cells. Limitations: Engineered expression; not a human organ concentration. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_access

Primary abstract

experimental_model

Human monocytic cell culture.

limitations

No unique HAT isoform or direct binding site was resolved in the abstract.

nutrient_topic

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

plain_language

Chromatin-regulating activity accompanied the inflammatory response.

primary_references

Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 448–454

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human monocytic cell culture. · source_derived_draft · unverified_draft

## fisetin-histone-enzyme-response Chromatin-regulating activity accompanied the inflammatory response. Fisetin, luteolin and combination treatments reduced histone-acetyltransferase activity in high-glucose-treated human THP-1 cells. Model: Human monocytic cell culture. Limitations: No unique HAT isoform or direct binding site was resolved in the abstract. Evidence access: Primary abstract Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968

evidence_access

Primary abstract

experimental_model

Fisetin, luteolin and combination conditions in human cells.

limitations

Expression is not proven direct SIRT1 activation or greater NAD availability.

nutrient_topic

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

plain_language

This branch connects to NAD-dependent cell regulation.

primary_references

Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 456–462

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fisetin, luteolin and combination conditions in human cells. · source_derived_draft · unverified_draft

## fisetin-sirt1-foxo-response This branch connects to NAD-dependent cell regulation. The THP-1 treatments increased SIRT1 and FOXO3a expression while suppressing high-glucose inflammatory responses. Model: Fisetin, luteolin and combination conditions in human cells. Limitations: Expression is not proven direct SIRT1 activation or greater NAD availability. Evidence access: Primary abstract Combination Treatments with Luteolin and Fisetin Enhance Anti-Inflammatory Effects in High Glucose-Treated THP-1 Cells Through Histone Acetyltransferase/Histone Deacetylase Regulation. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28650731/ · DOI 10.1089/jmf.2017.3968