Nutrient chapter

Anthocyanins

A diverse class of glycosylated pigments. Experimental actors, preparations, metabolites and compartments are recorded separately; class membership does not transfer effects. Human exposure, vascular, intestinal, metabolic and cross-nutrient mechanisms with null findings and open questions.

88 recorded mechanisms · 3 availability situations · 1 preserved sources. Source recording and scientific verification are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

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

The anthocyanin class includes Cyanidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.
Anthocyanins → Cyanidin 3-O-beta-D-glucopyranoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Cyanidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.
primary_references
Molecular Mechanisms Underlying the Absorption of Aglycone and Glycosidic Flavonoids in a Caco-2 BBe1 Cell Model. | 2020 | DOI 10.1021/acsomega.0c00379 | PMID 32455198 | https://pubmed.ncbi.nlm.nih.gov/32455198/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/ | https://doi.org/10.1021/acsomega.0c00379
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Cyanidin 3-O-beta-D-galactopyranoside; membership does not transfer experimental effects.
Anthocyanins → Cyanidin 3-O-beta-D-galactopyranoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Cyanidin 3-O-beta-D-galactopyranoside; membership does not transfer experimental effects.
primary_references
Investigating the Interaction of Ascorbic Acid with Anthocyanins and Pyranoanthocyanins. | 2018 | DOI 10.3390/molecules23040744 | PMID 29570649 | https://pubmed.ncbi.nlm.nih.gov/29570649/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6017693/ | https://doi.org/10.3390/molecules23040744
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Cyanidin 3,5-O-diglucoside / cyanin; membership does not transfer experimental effects.
Anthocyanins → Cyanidin 3,5-O-diglucoside / cyanin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Cyanidin 3,5-O-diglucoside / cyanin; membership does not transfer experimental effects.
primary_references
Molecular Mechanisms Underlying the Absorption of Aglycone and Glycosidic Flavonoids in a Caco-2 BBe1 Cell Model. | 2020 | DOI 10.1021/acsomega.0c00379 | PMID 32455198 | https://pubmed.ncbi.nlm.nih.gov/32455198/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/ | https://doi.org/10.1021/acsomega.0c00379
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Delphinidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.
Anthocyanins → Delphinidin 3-O-beta-D-glucopyranoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Delphinidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Malvidin 3-O-glucoside; membership does not transfer experimental effects.
Anthocyanins → Malvidin 3-O-glucoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Malvidin 3-O-glucoside; membership does not transfer experimental effects.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Peonidin 3-O-glucoside; membership does not transfer experimental effects.
Anthocyanins → Peonidin 3-O-glucoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Peonidin 3-O-glucoside; membership does not transfer experimental effects.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The anthocyanin class includes Petunidin 3-O-glucoside; membership does not transfer experimental effects.
Anthocyanins → Petunidin 3-O-glucoside Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Chemical classification, not an intervention or efficacy result.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Glycosides remain separate from aglycones and from each other. This neutral identity record is navigation, not a signed causal mechanism.
plain_language
The anthocyanin class includes Petunidin 3-O-glucoside; membership does not transfer experimental effects.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 7-7; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 7–7
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical classification, not an intervention or efficacy result. · Recorded from source · Recorded from source
Anthocyanins are a class of glycosylated pigments, not one circulating drug. Their anthocyanidin cores include cyanidin, delphinidin, pelargonidin, peonidin, petunidin and malvidin. Sugar position, sugar identity, methylation and acylation change their behavior. Cyanidin, cyanidin-3-O-glucoside, cyanidin-3-O-galactoside and cyanidin-3,5-O-diglucoside are separate molecules. Nasunin is a distinct acylated delphinidin glycoside; it must not inherit every result obtained with cyanidin-3-glucoside. The tested aglycones and glycosides illustrate why the individual structures matter. [Purified-compound comparison](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Blueberry polyphenol drink in acute vascular studies Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Intake and time dependence of blueberry flavonoid-induced improvements in vascular function: a randomized, controlled, double-blind, crossover intervention study with mechanistic insights into biological activity. | 2013 | DOI 10.3945/ajcn.113.066639 | PMID 24004888 | https://pubmed.ncbi.nlm.nih.gov/24004888/ | https://doi.org/10.3945/ajcn.113.066639
source_locator
Reviewed reference lines 54-54; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 54–54
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Blueberry FMD timing tracks a changing exposure.** Acute crossover experiments in healthy men found FMD increases at 1–2 and six hours, associated with circulating phenolics and lower neutrophil NADPH-oxidase activity. A plateau occurred above roughly 766 mg of total blueberry polyphenols in that protocol. This was neither 766 mg purified anthocyanins nor a universal optimum. Neutrophil measurements cannot be relabeled direct endothelial NOX inhibition. [Rodriguez-Mateos et al., 2013](https://pubmed.ncbi.nlm.nih.gov/24004888/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Wild blueberry powder preparation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Characterization of Wild Blueberry Polyphenols Bioavailability and Kinetic Profile in Plasma over 24-h Period in Human Subjects. | 2017 | DOI 10.1002/mnfr.201700405 | PMID 28887907 | https://pubmed.ncbi.nlm.nih.gov/28887907/ | https://doi.org/10.1002/mnfr.201700405
source_locator
Reviewed reference lines 32-32; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 32–32
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Whole-blueberry kinetics differ from a purified bolus.** In a meal-associated crossover study using 25 g freeze-dried wild-blueberry powder, parent anthocyanins peaked around two hours; individual glucuronide profiles peaked later, and phenolic acids ranged from early to late peaks. The reported anthocyanin bioavailability estimate was 1.1% under that study's method. It cannot replace the differently defined isotope-recovery measure or establish a class-wide absolute absorption percentage. [Zhong et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28887907/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Blueberry powder standardized to half- or one-cup equivalents in Curtis 2019 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Blueberries improve biomarkers of cardiometabolic function in participants with metabolic syndrome-results from a 6-month, double-blind, randomized controlled trial. | 2019 | DOI 10.1093/ajcn/nqy380 | PMID 31136659 | https://pubmed.ncbi.nlm.nih.gov/31136659/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/ | https://doi.org/10.1093/ajcn/nqy380
source_locator
Reviewed reference lines 62-62; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 62–62
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Clinical nulls remain part of the mechanism reference.** In 115 adults with metabolic syndrome completing a six-month randomized blueberry trial, one-cup-equivalent intake improved FMD, but insulin resistance, blood pressure, pulse-wave velocity, NO and overall plasma thiol status did not significantly improve. Half-cup-equivalent intake did not improve the reported biomarkers. These results do not contradict every short-term purified-compound study; they constrain extrapolation across preparations, durations and endpoints. [Curtis et al., 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/). Its corrigendum changes the insulin unit in Table 2 to mU/L; it does not announce a reversal of the trial's outcomes. [Publisher correction](https://pmc.ncbi.nlm.nih.gov/articles/PMC6821540/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Bilberry extract with 25% anthocyanosides in Muth 2000 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
The effect of bilberry nutritional supplementation on night visual acuity and contrast sensitivity. | 2000 | PMID 10767671 | https://pubmed.ncbi.nlm.nih.gov/10767671/
source_locator
Reviewed reference lines 98-98; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 98–98
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Controlled human night-vision results were negative.** A 15-man crossover trial used 160 mg bilberry extract containing 25% anthocyanosides three times daily for 21 days, with a washout and crossover. Night visual acuity and contrast sensitivity did not improve versus placebo. This constrains that preparation in healthy young men; it is not a finding about all eye diseases. Wartime anecdotes are not substitutes for this comparison. [Muth et al., 2000](https://pubmed.ncbi.nlm.nih.gov/10767671/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Blackcurrant anthocyanin preparation in Matsumoto 2006 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Comparative assessment of distribution of blackcurrant anthocyanins in rabbit and rat ocular tissues. | 2006 | DOI 10.1016/j.exer.2005.12.019 | PMID 16635490 | https://pubmed.ncbi.nlm.nih.gov/16635490/ | https://doi.org/10.1016/j.exer.2005.12.019
source_locator
Reviewed reference lines 96-96; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 96–96
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Animal ocular delivery has been observed.** Blackcurrant anthocyanins were detected intact in rat and rabbit ocular tissues after the reported oral and injected administrations. Route and species matter: these experiments cannot establish a human retinal concentration after eating berries, an equivalence to vitamin A, or enhanced rhodopsin regeneration in people. [Matsumoto et al., 2006](https://pubmed.ncbi.nlm.nih.gov/16635490/).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Ten standardized elderberry fruit extracts in Mladenka 2016 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
Anthocyanins → Anthocyanin preparations tested in human fecal incubations Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Preparation identity/scope; not isolated class causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
A food or extract contains other constituents. Membership is a navigation link and does not transfer its findings to isolated anthocyanins.
plain_language
The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.
primary_references
Stability and biotransformation of various dietary anthocyanins in vitro. | 2006 | DOI 10.1007/s00394-005-0557-8 | PMID 15834757 | https://pubmed.ncbi.nlm.nih.gov/15834757/ | https://doi.org/10.1007/s00394-005-0557-8
source_locator
Reviewed reference lines 44-44; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 44–44
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Preparation identity/scope; not isolated class causation. · Recorded from source · Recorded from source
**Microbial cleavage and host conjugation are distinct steps.** Anaerobic human fecal incubations degraded glycosylated and acylated anthocyanins to B-ring-derived phenolic acids. Separate rat-liver microsome experiments produced glucuronides when supplied with activated glucuronic acid; the tested NADPH-supported P450 system did not hydroxylate or demethylate the pigments. These are model-specific positive and negative findings, not proof that all human metabolism is exclusively microbial or that every CYP interaction is absent. [Keppler and Humpf, 2005](https://pubmed.ncbi.nlm.nih.gov/15834757/).
Complete structured claim and evidence
The tested signatures reconstruct serum metabolite profiles measured after labeled C3G exposure; they are separate mixtures, not intact C3G.
Cyanidin 3-O-beta-D-glucopyranoside → Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
In vitro mixtures reconstructed with authentic standards from a human tracer cohort.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation provenance does not attribute every component effect to the parent or transfer unrelated metabolite findings.
plain_language
The tested signatures reconstruct serum metabolite profiles measured after labeled C3G exposure; they are separate mixtures, not intact C3G.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · In vitro mixtures reconstructed with authentic standards from a human tracer cohort. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
Solution pH changes reversible molecular-form transitions of the tested anthocyanin glucosides; degradation is a separate process.
Cyanidin 3-O-beta-D-glucopyranoside → Anthocyanin pH-dependent reversible molecular-form transitions Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Purified anthocyanin aqueous-solution kinetics; exact compound and pH dependence.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Solution pH changes reversible molecular-form transitions of the tested anthocyanin glucosides; degradation is a separate process.
primary_references
A New Insight into the Degradation of Anthocyanins: Reversible versus the Irreversible Chemical Processes. | 2022 | DOI 10.1021/acs.jafc.1c06521 | PMID 34982560 | https://pubmed.ncbi.nlm.nih.gov/34982560/ | https://doi.org/10.1021/acs.jafc.1c06521
source_locator
Reviewed reference lines 11-11; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 11–11
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified anthocyanin aqueous-solution kinetics; exact compound and pH dependence. · Recorded from source · Recorded from source
**pH changes molecular form.** Experiments with four purified 3-O-glucosides distinguish reversible proton transfer, hydration and cis/trans isomerization from irreversible degradation. Flavylium, quinoidal, hemiketal and chalcone states are a reaction network whose populations and rates depend on the particular compound and solution. Color loss alone cannot identify the reaction. Neither one universal form at blood pH nor one universal plasma half-life follows from these solution experiments. [Sousa and colleagues, 2022](https://pubmed.ncbi.nlm.nih.gov/34982560/).
Complete structured claim and evidence
Anthocyanin structure changes parent stability during DMEM incubation at pH 7.4, 37 C and 5% CO2.
Cyanidin 3-O-beta-D-glucopyranoside → Anthocyanin parent loss during culture-medium incubation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Ten-compound chemical stability study in DMEM and water.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Relative structural trends; no common plasma half-life or exact intracellular exposure inferred.
plain_language
Anthocyanin structure changes parent stability during DMEM incubation at pH 7.4, 37 C and 5% CO2.
primary_references
Structure-stability relationship of anthocyanins under cell culture condition. | 2019 | DOI 10.1080/09637486.2018.1506753 | PMID 30160540 | https://pubmed.ncbi.nlm.nih.gov/30160540/ | https://doi.org/10.1080/09637486.2018.1506753
source_locator
Reviewed reference lines 13-13; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 13–13
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Ten-compound chemical stability study in DMEM and water. · Recorded from source · Recorded from source
**Culture medium changes the exposure.** A ten-compound study in DMEM at 37 °C, pH 7.4 and 5% CO2 found structure-dependent losses: glycosylation and B-ring methylation generally improved stability, while additional B-ring hydroxylation reduced it. Water and DMEM were not interchangeable. A nominal parent-compound dose maintained for hours may become a changing mixture; chemical measurements should accompany the biological assay. A flavylium charge under acidic conditions also does not establish selective mitochondrial delivery in living humans. [Zhang and colleagues, 2018](https://pubmed.ncbi.nlm.nih.gov/30160540/).
Complete structured claim and evidence
After 500 mg labeled C3G in eight men, urine plus breath contained 12.38% of administered label over 48 hours; this is not intact C3G recovery.
Cyanidin 3-O-beta-D-glucopyranoside → Recovery of orally administered C3G-derived isotope in human urine and breath Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Eight healthy men, single oral 500 mg 13C5-C3G, 48-hour sampling.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
After 500 mg labeled C3G in eight men, urine plus breath contained 12.38% of administered label over 48 hours; this is not intact C3G recovery.
primary_references
Human metabolism and elimination of the anthocyanin, cyanidin-3-glucoside: a (13)C-tracer study. | 2013 | DOI 10.3945/ajcn.112.049247 | PMID 23604435 | https://pubmed.ncbi.nlm.nih.gov/23604435/ | https://doi.org/10.3945/ajcn.112.049247
source_locator
Reviewed reference lines 17-17; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 17–17
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Eight healthy men, single oral 500 mg 13C5-C3G, 48-hour sampling. · Recorded from source · Recorded from source
**Tracer recovery is not intact-pigment bioavailability.** Eight men received 500 mg of isotopically labeled cyanidin-3-glucoside (C3G), with sampling over 48 hours. The reported 12.38 ± 1.38% relative bioavailability comprised labeled carbon recovered in urine and breath: 5.37 ± 0.67% and 6.91 ± 1.59%, respectively. It is not 12.38% intact C3G, nor 12.38% pharmacologically active material. Combined labeled serum metabolites peaked at approximately 5.97 µM around 10.25 hours. Low urinary recovery of unchanged pigment cannot quantify total absorption. [Czank et al., 2013](https://pubmed.ncbi.nlm.nih.gov/23604435/).
Complete structured claim and evidence
The tracer cohort had mean serum C3G Cmax 141 +/- 70 nM at 1.8 +/- 0.2 hours, measurable in five participants.
Cyanidin 3-O-beta-D-glucopyranoside → Human serum intact cyanidin-3-glucoside concentration Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Same eight-men cohort as Czank 2013; analyte-specific n=5, mean +/- SEM.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The tracer cohort had mean serum C3G Cmax 141 +/- 70 nM at 1.8 +/- 0.2 hours, measurable in five participants.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same eight-men cohort as Czank 2013; analyte-specific n=5, mean +/- SEM. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
Labeled C3G produced circulating labeled PCA in humans; mean free PCA Cmax was 146 +/- 74 nM, n=8.
Cyanidin 3-O-beta-D-glucopyranoside → Protocatechuic acid / 3,4-dihydroxybenzoic acid Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Human 500 mg labeled C3G bolus; plasma chemical measurement, not a biological efficacy test.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Specific tracer-supported precursor/product relationship; does not assign every PCA effect to C3G or identify all microbial versus nonmicrobial formation.
plain_language
Labeled C3G produced circulating labeled PCA in humans; mean free PCA Cmax was 146 +/- 74 nM, n=8.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human 500 mg labeled C3G bolus; plasma chemical measurement, not a biological efficacy test. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
After labeled C3G ingestion, Protocatechuic-acid sulfate isomers, unresolved assay sum was detected as a labeled serum product with its own concentration-time profile.
Cyanidin 3-O-beta-D-glucopyranoside → Protocatechuic-acid sulfate isomers, unresolved assay sum Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Tracer-derived product, not sole active payload. Different maxima cannot be summed into a simultaneous mixture. Shared metabolites retain independent identity and effects.
plain_language
After labeled C3G ingestion, Protocatechuic-acid sulfate isomers, unresolved assay sum was detected as a labeled serum product with its own concentration-time profile.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
After labeled C3G ingestion, Vanillic acid / 4-hydroxy-3-methoxybenzoic acid was detected as a labeled serum product with its own concentration-time profile.
Cyanidin 3-O-beta-D-glucopyranoside → Vanillic acid / 4-hydroxy-3-methoxybenzoic acid Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Tracer-derived product, not sole active payload. Different maxima cannot be summed into a simultaneous mixture. Shared metabolites retain independent identity and effects.
plain_language
After labeled C3G ingestion, Vanillic acid / 4-hydroxy-3-methoxybenzoic acid was detected as a labeled serum product with its own concentration-time profile.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
After labeled C3G ingestion, Ferulic acid / 4-hydroxy-3-methoxycinnamic acid was detected as a labeled serum product with its own concentration-time profile.
Cyanidin 3-O-beta-D-glucopyranoside → Ferulic acid / 4-hydroxy-3-methoxycinnamic acid Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Tracer-derived product, not sole active payload. Different maxima cannot be summed into a simultaneous mixture. Shared metabolites retain independent identity and effects.
plain_language
After labeled C3G ingestion, Ferulic acid / 4-hydroxy-3-methoxycinnamic acid was detected as a labeled serum product with its own concentration-time profile.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
After labeled C3G ingestion, Hippuric acid / benzoylglycine was detected as a labeled serum product with its own concentration-time profile.
Cyanidin 3-O-beta-D-glucopyranoside → Hippuric acid / benzoylglycine Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_model
Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Tracer-derived product, not sole active payload. Different maxima cannot be summed into a simultaneous mixture. Shared metabolites retain independent identity and effects.
plain_language
After labeled C3G ingestion, Hippuric acid / benzoylglycine was detected as a labeled serum product with its own concentration-time profile.
primary_references
The pharmacokinetics of anthocyanins and their metabolites in humans. | 2014 | DOI 10.1111/bph.12676 | PMID 24602005 | https://pubmed.ncbi.nlm.nih.gov/24602005/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/ | https://doi.org/10.1111/bph.12676
source_locator
Reviewed reference lines 19-30; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 19–30
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same human 500 mg tracer cohort; refer to the analyte-specific n, pooled isomers and peak times in Table 2. · Recorded from source · Recorded from source
**Individual metabolites peak at different times.** A second analysis of the same tracer cohort reported the following selected serum values; these are means ± SEM, not universal target concentrations. The number of participants with quantifiable analyte differed by compound. [de Ferrars et al., 2014, Table 2](https://pmc.ncbi.nlm.nih.gov/articles/PMC4080980/). | Analyte | n | Peak, nM | Time to peak, hours | |---|---:|---:|---:| | C3G | 5 | 141 ± 70 | 1.8 ± 0.2 | | Protocatechuic acid (PCA) | 8 | 146 ± 74 | 3.3 ± 0.7 | | PCA sulfates, pooled isomers | 8 | 157 ± 116 | 11.4 ± 3.8 | | Vanillic acid | 2 | 1,845 ± 838 | 12.5 ± 11.5 | | Ferulic acid, B-ring label | 7 | 827 ± 371 | 8.2 ± 4.1 | | Hippuric acid | 8 | 1,962 ± 1,389 | 15.7 ± 4.1 | Free PCA and C3G therefore had similar mean peaks in this experiment. Vanillic acid's estimate came from only two participants. The values are distinct maxima, not a simultaneous mixture to be summed. Conjugated and unconjugated forms are separate exposures. A 50 µM PCA experiment is roughly 340 times this mean free-PCA peak; plasma comparisons still do not establish intestinal or intracellular concentrations. The two tracer publications are complementary analyses, not independent replications.
Complete structured claim and evidence
After the tested blueberry meal, parent anthocyanins peaked earlier than several glucuronides and phenolic products.
Wild blueberry powder preparation → Human serum C3G and metabolite concentration-time profiles Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Human crossover meal study, 25 g freeze-dried wild-blueberry powder, 24-hour plasma sampling.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
After the tested blueberry meal, parent anthocyanins peaked earlier than several glucuronides and phenolic products.
primary_references
Characterization of Wild Blueberry Polyphenols Bioavailability and Kinetic Profile in Plasma over 24-h Period in Human Subjects. | 2017 | DOI 10.1002/mnfr.201700405 | PMID 28887907 | https://pubmed.ncbi.nlm.nih.gov/28887907/ | https://doi.org/10.1002/mnfr.201700405
source_locator
Reviewed reference lines 32-32; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 32–32
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human crossover meal study, 25 g freeze-dried wild-blueberry powder, 24-hour plasma sampling. · Recorded from source · Recorded from source
**Whole-blueberry kinetics differ from a purified bolus.** In a meal-associated crossover study using 25 g freeze-dried wild-blueberry powder, parent anthocyanins peaked around two hours; individual glucuronide profiles peaked later, and phenolic acids ranged from early to late peaks. The reported anthocyanin bioavailability estimate was 1.1% under that study's method. It cannot replace the differently defined isotope-recovery measure or establish a class-wide absolute absorption percentage. [Zhong et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28887907/).
Complete structured claim and evidence
Knocking down SLC5A1 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.
Cyanidin 3-O-beta-D-glucopyranoside → C3G transport across differentiated human Caco-2 monolayers Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
C3G exposure with scrambled siRNA present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
C3G exposure with scrambled siRNA siRNA knockdown · Human sodium/glucose cotransporter SGLT1 / SLC5A1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G exposure with SLC5A1 siRNA", "comparator": "C3G exposure with scrambled siRNA", "endpoint": "Knocking down SLC5A1 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "slc5a1", "state": "siRNA knockdown"}, {"entity_slug": "cyanidin-3-glucoside", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2; 10-40 uM C3G transport experiments up to 120 min; siRNA comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Knockdown result, not a wild-type inhibitory action of the transporter. Does not quantify its contribution to human in vivo absorption.
plain_language
Knocking down SLC5A1 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.
primary_references
The role of sodium-dependent glucose transporter 1 and glucose transporter 2 in the absorption of cyanidin-3-o-β-glucoside in Caco-2 cells. | 2014 | DOI 10.3390/nu6104165 | PMID 25314643 | https://pubmed.ncbi.nlm.nih.gov/25314643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4210911/ | https://doi.org/10.3390/nu6104165
source_locator
Reviewed reference lines 38-38; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 38–38
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2; 10-40 uM C3G transport experiments up to 120 min; siRNA comparison. · Recorded from source · Recorded from source
**SGLT1 and GLUT2 have experimental support.** In differentiated human Caco-2 monolayers, pharmacological inhibition and separate SGLT1 or GLUT2 siRNA reduced C3G transport. Transport was examined across 10–40 µM C3G and up to 120 minutes; scrambled siRNA provided a comparator. This supports involvement in that epithelial model, not an exclusive absorption route or a measured contribution in the human intestine. Canonical proteins are SLC5A1/SGLT1 and SLC2A2/GLUT2. [Zou et al., 2014](https://pmc.ncbi.nlm.nih.gov/articles/PMC4210911/).
Complete structured claim and evidence
Knocking down SLC2A2 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.
Cyanidin 3-O-beta-D-glucopyranoside → C3G transport across differentiated human Caco-2 monolayers Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
C3G exposure with scrambled siRNA siRNA knockdown · Human glucose transporter 2 / SLC2A2 / GLUT2 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
C3G exposure with scrambled siRNA present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G exposure with SLC2A2 siRNA", "comparator": "C3G exposure with scrambled siRNA", "endpoint": "Knocking down SLC2A2 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "slc2a2", "state": "siRNA knockdown"}, {"entity_slug": "cyanidin-3-glucoside", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2; 10-40 uM C3G transport experiments up to 120 min; siRNA comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Knockdown result, not a wild-type inhibitory action of the transporter. Does not quantify its contribution to human in vivo absorption.
plain_language
Knocking down SLC2A2 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.
primary_references
The role of sodium-dependent glucose transporter 1 and glucose transporter 2 in the absorption of cyanidin-3-o-β-glucoside in Caco-2 cells. | 2014 | DOI 10.3390/nu6104165 | PMID 25314643 | https://pubmed.ncbi.nlm.nih.gov/25314643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4210911/ | https://doi.org/10.3390/nu6104165
source_locator
Reviewed reference lines 38-38; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 38–38
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2; 10-40 uM C3G transport experiments up to 120 min; siRNA comparison. · Recorded from source · Recorded from source
**SGLT1 and GLUT2 have experimental support.** In differentiated human Caco-2 monolayers, pharmacological inhibition and separate SGLT1 or GLUT2 siRNA reduced C3G transport. Transport was examined across 10–40 µM C3G and up to 120 minutes; scrambled siRNA provided a comparator. This supports involvement in that epithelial model, not an exclusive absorption route or a measured contribution in the human intestine. Canonical proteins are SLC5A1/SGLT1 and SLC2A2/GLUT2. [Zou et al., 2014](https://pmc.ncbi.nlm.nih.gov/articles/PMC4210911/).
Complete structured claim and evidence
The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.
Cyanidin 3-O-beta-D-glucopyranoside → 2-NBDG uptake by human Caco-2 BBe1 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "50 uM cyanidin-3-glucoside", "comparator": "Cell assay without added glycoside", "endpoint": "The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Caco-2 BBe1; 50 uM flavonoid pretreatment, fluorescent 2-NBDG uptake; not dietary human glucose absorption.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Fluorescent analogue outcome, not verified clinical glycemic benefit or carbohydrate deficiency.
plain_language
The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.
primary_references
Molecular Mechanisms Underlying the Absorption of Aglycone and Glycosidic Flavonoids in a Caco-2 BBe1 Cell Model. | 2020 | DOI 10.1021/acsomega.0c00379 | PMID 32455198 | https://pubmed.ncbi.nlm.nih.gov/32455198/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/ | https://doi.org/10.1021/acsomega.0c00379
source_locator
Reviewed reference lines 40-40; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 40–40
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Caco-2 BBe1; 50 uM flavonoid pretreatment, fluorescent 2-NBDG uptake; not dietary human glucose absorption. · Recorded from source · Recorded from source
**Glucose handling is a separate cross-nutrient interaction.** A Caco-2 BBe1 study tested cyanidin and glycosides alongside quercetin compounds. At 50 µM, the glycosides reduced uptake of the fluorescent glucose analogue 2-NBDG. Transport inhibition and SGLT1 knockdown supported carrier involvement in glycoside uptake, with different behavior for aglycones. This is a nutrient-transport interaction in cultured cells; it is not proof that ordinary berry intake blocks intestinal glucose absorption or causes carbohydrate deficiency. [Zhang et al., 2020, transport and glucose-uptake experiments](https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/).
Complete structured claim and evidence
The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.
Cyanidin 3,5-O-diglucoside / cyanin → 2-NBDG uptake by human Caco-2 BBe1 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "50 uM cyanidin-3-5-diglucoside", "comparator": "Cell assay without added glycoside", "endpoint": "The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Caco-2 BBe1; 50 uM flavonoid pretreatment, fluorescent 2-NBDG uptake; not dietary human glucose absorption.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Fluorescent analogue outcome, not verified clinical glycemic benefit or carbohydrate deficiency.
plain_language
The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.
primary_references
Molecular Mechanisms Underlying the Absorption of Aglycone and Glycosidic Flavonoids in a Caco-2 BBe1 Cell Model. | 2020 | DOI 10.1021/acsomega.0c00379 | PMID 32455198 | https://pubmed.ncbi.nlm.nih.gov/32455198/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/ | https://doi.org/10.1021/acsomega.0c00379
source_locator
Reviewed reference lines 40-40; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 40–40
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Caco-2 BBe1; 50 uM flavonoid pretreatment, fluorescent 2-NBDG uptake; not dietary human glucose absorption. · Recorded from source · Recorded from source
**Glucose handling is a separate cross-nutrient interaction.** A Caco-2 BBe1 study tested cyanidin and glycosides alongside quercetin compounds. At 50 µM, the glycosides reduced uptake of the fluorescent glucose analogue 2-NBDG. Transport inhibition and SGLT1 knockdown supported carrier involvement in glycoside uptake, with different behavior for aglycones. This is a nutrient-transport interaction in cultured cells; it is not proof that ordinary berry intake blocks intestinal glucose absorption or causes carbohydrate deficiency. [Zhang et al., 2020, transport and glucose-uptake experiments](https://pmc.ncbi.nlm.nih.gov/articles/PMC7240828/).
Complete structured claim and evidence
The tested anthocyanin structures competed in a bilitranslocase transport assay; the class result was 17 of 20 compounds, Ki 1.4-22 uM.
Cyanidin 3-O-beta-D-galactopyranoside → Bilitranslocase carrier activity in the 2002 assay; gene assignment unresolved Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Test anthocyanin addition", "comparator": "Carrier assay without added anthocyanin", "endpoint": "The tested anthocyanin structures competed in a bilitranslocase transport assay; the class result was 17 of 20 compounds, Ki 1.4-22 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free membrane-carrier transport inhibition assay; individual constants not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Competition supports interaction, not a complete human absorption mechanism or an inferred transporter-gene identity.
plain_language
The tested anthocyanin structures competed in a bilitranslocase transport assay; the class result was 17 of 20 compounds, Ki 1.4-22 uM.
primary_references
The interaction of anthocyanins with bilitranslocase. | 2002 | DOI 10.1016/s0006-291x(02)00927-0 | PMID 12176028 | https://pubmed.ncbi.nlm.nih.gov/12176028/ | https://doi.org/10.1016/s0006-291x(02)00927-0 | https://doi.org/10.1016/S0006-291X%2802%2900927-0
source_locator
Reviewed reference lines 42-42; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 42–42
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free membrane-carrier transport inhibition assay; individual constants not extracted. · Recorded from source · Recorded from source
**Bilitranslocase remains a candidate route.** Seventeen of twenty tested anthocyanin-related compounds competitively inhibited a bilitranslocase transport assay, with reported inhibition constants of 1.4–22 µM. Glycosylated compounds often interacted more strongly than their aglycones. Competition in a carrier assay is useful evidence, but does not determine how much pigment crosses the human stomach. The assay-associated carrier should not be silently assigned an unrelated established transporter gene. [Passamonti et al., 2002](https://doi.org/10.1016/S0006-291X%2802%2900927-0).
Complete structured claim and evidence
Human fecal microbiota degraded the tested anthocyanins in anaerobic incubations, producing B-ring phenolic acids.
Anthocyanin preparations tested in human fecal incubations → Anaerobic human fecal-microbiota anthocyanin degradation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Anaerobic in vitro human fecal suspension; composition and source-specific structures matter.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Human fecal microbiota degraded the tested anthocyanins in anaerobic incubations, producing B-ring phenolic acids.
primary_references
Stability and biotransformation of various dietary anthocyanins in vitro. | 2006 | DOI 10.1007/s00394-005-0557-8 | PMID 15834757 | https://pubmed.ncbi.nlm.nih.gov/15834757/ | https://doi.org/10.1007/s00394-005-0557-8
source_locator
Reviewed reference lines 44-44; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 44–44
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Anaerobic in vitro human fecal suspension; composition and source-specific structures matter. · Recorded from source · Recorded from source
**Microbial cleavage and host conjugation are distinct steps.** Anaerobic human fecal incubations degraded glycosylated and acylated anthocyanins to B-ring-derived phenolic acids. Separate rat-liver microsome experiments produced glucuronides when supplied with activated glucuronic acid; the tested NADPH-supported P450 system did not hydroxylate or demethylate the pigments. These are model-specific positive and negative findings, not proof that all human metabolism is exclusively microbial or that every CYP interaction is absent. [Keppler and Humpf, 2005](https://pubmed.ncbi.nlm.nih.gov/15834757/).
Complete structured claim and evidence
Separate rat microsomal experiments glucuronidated anthocyanins when activated glucuronic acid was supplied.
Anthocyanin preparations tested in human fecal incubations → Anthocyanin glucuronidation in rat liver microsomes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Rat liver microsomes with activated glucuronic acid; no inference to a specific human UGT isoform.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Separate rat microsomal experiments glucuronidated anthocyanins when activated glucuronic acid was supplied.
primary_references
Stability and biotransformation of various dietary anthocyanins in vitro. | 2006 | DOI 10.1007/s00394-005-0557-8 | PMID 15834757 | https://pubmed.ncbi.nlm.nih.gov/15834757/ | https://doi.org/10.1007/s00394-005-0557-8
source_locator
Reviewed reference lines 44-44; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 44–44
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat liver microsomes with activated glucuronic acid; no inference to a specific human UGT isoform. · Recorded from source · Recorded from source
**Microbial cleavage and host conjugation are distinct steps.** Anaerobic human fecal incubations degraded glycosylated and acylated anthocyanins to B-ring-derived phenolic acids. Separate rat-liver microsome experiments produced glucuronides when supplied with activated glucuronic acid; the tested NADPH-supported P450 system did not hydroxylate or demethylate the pigments. These are model-specific positive and negative findings, not proof that all human metabolism is exclusively microbial or that every CYP interaction is absent. [Keppler and Humpf, 2005](https://pubmed.ncbi.nlm.nih.gov/15834757/).
Complete structured claim and evidence
The tested NADPH-supported rat microsomal P450 system did not detect anthocyanin hydroxylation or demethylation.
Anthocyanin preparations tested in human fecal incubations → Anthocyanin hydroxylation and demethylation in the tested rat microsomal P450 assay Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Anthocyanins with NADPH-supported microsomal oxidation system", "comparator": "Assay baseline parent/product profile", "endpoint": "The tested NADPH-supported rat microsomal P450 system did not detect anthocyanin hydroxylation or demethylation.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat liver microsomes; NADPH-supported phase-I assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No detected metabolism in this assay; not absence of every CYP-mediated reaction or drug interaction.
plain_language
The tested NADPH-supported rat microsomal P450 system did not detect anthocyanin hydroxylation or demethylation.
primary_references
Stability and biotransformation of various dietary anthocyanins in vitro. | 2006 | DOI 10.1007/s00394-005-0557-8 | PMID 15834757 | https://pubmed.ncbi.nlm.nih.gov/15834757/ | https://doi.org/10.1007/s00394-005-0557-8
source_locator
Reviewed reference lines 44-44; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 44–44
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat liver microsomes; NADPH-supported phase-I assay. · Recorded from source · Recorded from source
**Microbial cleavage and host conjugation are distinct steps.** Anaerobic human fecal incubations degraded glycosylated and acylated anthocyanins to B-ring-derived phenolic acids. Separate rat-liver microsome experiments produced glucuronides when supplied with activated glucuronic acid; the tested NADPH-supported P450 system did not hydroxylate or demethylate the pigments. These are model-specific positive and negative findings, not proof that all human metabolism is exclusively microbial or that every CYP interaction is absent. [Keppler and Humpf, 2005](https://pubmed.ncbi.nlm.nih.gov/15834757/).
Complete structured claim and evidence
The 12-week purified berry anthocyanin trial reported higher brachial FMD versus placebo.
Purified berry anthocyanin mixture in Zhu 2011 → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "320 mg/day purified berry anthocyanin mixture", "comparator": "Placebo for 12 weeks", "endpoint": "The 12-week purified berry anthocyanin trial reported higher brachial FMD versus placebo.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The 12-week purified berry anthocyanin trial reported higher brachial FMD versus placebo.
primary_references
Purified anthocyanin supplementation improves endothelial function via NO-cGMP activation in hypercholesterolemic individuals. | 2011 | DOI 10.1373/clinchem.2011.167361 | PMID 21926181 | https://pubmed.ncbi.nlm.nih.gov/21926181/ | https://doi.org/10.1373/clinchem.2011.167361
source_locator
Reviewed reference lines 52-52; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 52–52
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled. · Recorded from source · Recorded from source
**Purified berry anthocyanins changed human vascular function.** A 2011 study included a 12-person acute crossover and a 150-person, 12-week trial of 320 mg/day. Flow-mediated dilation (FMD) and plasma cGMP improved; LDL cholesterol and soluble VCAM-1 decreased, with HDL cholesterol increasing. Additional inhibitor experiments in six people and rat aortic rings supported involvement of NO–cGMP signaling. The accessible abstract does not identify every inhibitor or its route, so this reference does not invent those details. FMD is vascular physiology, not proof of a particular parent molecule binding eNOS or prevention of cardiovascular events. [Zhu et al., 2011](https://pubmed.ncbi.nlm.nih.gov/21926181/).
Complete structured claim and evidence
The 12-week purified berry anthocyanin trial reported higher plasma cGMP versus placebo.
Purified berry anthocyanin mixture in Zhu 2011 → Human plasma cyclic GMP concentration Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "320 mg/day purified berry anthocyanin mixture", "comparator": "Placebo for 12 weeks", "endpoint": "The 12-week purified berry anthocyanin trial reported higher plasma cGMP versus placebo.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The 12-week purified berry anthocyanin trial reported higher plasma cGMP versus placebo.
primary_references
Purified anthocyanin supplementation improves endothelial function via NO-cGMP activation in hypercholesterolemic individuals. | 2011 | DOI 10.1373/clinchem.2011.167361 | PMID 21926181 | https://pubmed.ncbi.nlm.nih.gov/21926181/ | https://doi.org/10.1373/clinchem.2011.167361
source_locator
Reviewed reference lines 52-52; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 52–52
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled. · Recorded from source · Recorded from source
**Purified berry anthocyanins changed human vascular function.** A 2011 study included a 12-person acute crossover and a 150-person, 12-week trial of 320 mg/day. Flow-mediated dilation (FMD) and plasma cGMP improved; LDL cholesterol and soluble VCAM-1 decreased, with HDL cholesterol increasing. Additional inhibitor experiments in six people and rat aortic rings supported involvement of NO–cGMP signaling. The accessible abstract does not identify every inhibitor or its route, so this reference does not invent those details. FMD is vascular physiology, not proof of a particular parent molecule binding eNOS or prevention of cardiovascular events. [Zhu et al., 2011](https://pubmed.ncbi.nlm.nih.gov/21926181/).
Complete structured claim and evidence
The 12-week purified berry anthocyanin trial reported lower circulating soluble VCAM-1 versus placebo.
Purified berry anthocyanin mixture in Zhu 2011 → Human circulating soluble VCAM-1 concentration Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "320 mg/day purified berry anthocyanin mixture", "comparator": "Placebo for 12 weeks", "endpoint": "The 12-week purified berry anthocyanin trial reported lower circulating soluble VCAM-1 versus placebo.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The 12-week purified berry anthocyanin trial reported lower circulating soluble VCAM-1 versus placebo.
primary_references
Purified anthocyanin supplementation improves endothelial function via NO-cGMP activation in hypercholesterolemic individuals. | 2011 | DOI 10.1373/clinchem.2011.167361 | PMID 21926181 | https://pubmed.ncbi.nlm.nih.gov/21926181/ | https://doi.org/10.1373/clinchem.2011.167361
source_locator
Reviewed reference lines 52-52; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 52–52
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 150 hypercholesterolemic participants; 320 mg/day berry-isolated anthocyanins for 12 weeks, placebo-controlled. · Recorded from source · Recorded from source
**Purified berry anthocyanins changed human vascular function.** A 2011 study included a 12-person acute crossover and a 150-person, 12-week trial of 320 mg/day. Flow-mediated dilation (FMD) and plasma cGMP improved; LDL cholesterol and soluble VCAM-1 decreased, with HDL cholesterol increasing. Additional inhibitor experiments in six people and rat aortic rings supported involvement of NO–cGMP signaling. The accessible abstract does not identify every inhibitor or its route, so this reference does not invent those details. FMD is vascular physiology, not proof of a particular parent molecule binding eNOS or prevention of cardiovascular events. [Zhu et al., 2011](https://pubmed.ncbi.nlm.nih.gov/21926181/).
Complete structured claim and evidence
NO-cGMP inhibitor interventions abolished the reported anthocyanin-associated endothelial response in a small human experiment.
Purified berry anthocyanin mixture in Zhu 2011 → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_condition
Anthocyanin intervention without pathway inhibition administered · Purified berry anthocyanin mixture in Zhu 2011 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Anthocyanin intervention without pathway inhibition pharmacologically inhibited · The nitric oxide to soluble guanylate cyclase to cyclic GMP pathway Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Anthocyanin intervention in the presence of NO-cGMP inhibition", "comparator": "Anthocyanin intervention without pathway inhibition", "endpoint": "NO-cGMP inhibitor interventions abolished the reported anthocyanin-associated endothelial response in a small human experiment.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "berry-anthocyanins-zhu-2011", "state": "administered"}, {"entity_slug": "no-cgmp-pathway", "state": "pharmacologically inhibited"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Six-person human NO-cGMP inhibitor experiment, distinct from the 150-person trial and rat aortic-ring experiment.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Abstract-level extraction: exact human inhibitor, dose and route not verified. Does not demonstrate direct parent binding to eNOS.
plain_language
NO-cGMP inhibitor interventions abolished the reported anthocyanin-associated endothelial response in a small human experiment.
primary_references
Purified anthocyanin supplementation improves endothelial function via NO-cGMP activation in hypercholesterolemic individuals. | 2011 | DOI 10.1373/clinchem.2011.167361 | PMID 21926181 | https://pubmed.ncbi.nlm.nih.gov/21926181/ | https://doi.org/10.1373/clinchem.2011.167361
source_locator
Reviewed reference lines 52-52; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 52–52
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Six-person human NO-cGMP inhibitor experiment, distinct from the 150-person trial and rat aortic-ring experiment. · Recorded from source · Recorded from source
**Purified berry anthocyanins changed human vascular function.** A 2011 study included a 12-person acute crossover and a 150-person, 12-week trial of 320 mg/day. Flow-mediated dilation (FMD) and plasma cGMP improved; LDL cholesterol and soluble VCAM-1 decreased, with HDL cholesterol increasing. Additional inhibitor experiments in six people and rat aortic rings supported involvement of NO–cGMP signaling. The accessible abstract does not identify every inhibitor or its route, so this reference does not invent those details. FMD is vascular physiology, not proof of a particular parent molecule binding eNOS or prevention of cardiovascular events. [Zhu et al., 2011](https://pubmed.ncbi.nlm.nih.gov/21926181/).
Complete structured claim and evidence
Acute blueberry polyphenol intake was associated with lower neutrophil NADPH oxidase activity at times of improved FMD.
Blueberry polyphenol drink in acute vascular studies → Human neutrophil NADPH oxidase activity Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Blueberry polyphenol drink", "comparator": "Matched control drink", "endpoint": "Acute blueberry polyphenol intake was associated with lower neutrophil NADPH oxidase activity at times of improved FMD.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Healthy-men crossover studies; 1-2 and 6-hour sampling; measurements in neutrophils.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Neutrophil assay and temporal association; not direct endothelial NOX binding or proof of mediation.
plain_language
Acute blueberry polyphenol intake was associated with lower neutrophil NADPH oxidase activity at times of improved FMD.
primary_references
Intake and time dependence of blueberry flavonoid-induced improvements in vascular function: a randomized, controlled, double-blind, crossover intervention study with mechanistic insights into biological activity. | 2013 | DOI 10.3945/ajcn.113.066639 | PMID 24004888 | https://pubmed.ncbi.nlm.nih.gov/24004888/ | https://doi.org/10.3945/ajcn.113.066639
source_locator
Reviewed reference lines 54-54; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 54–54
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Healthy-men crossover studies; 1-2 and 6-hour sampling; measurements in neutrophils. · Recorded from source · Recorded from source
**Blueberry FMD timing tracks a changing exposure.** Acute crossover experiments in healthy men found FMD increases at 1–2 and six hours, associated with circulating phenolics and lower neutrophil NADPH-oxidase activity. A plateau occurred above roughly 766 mg of total blueberry polyphenols in that protocol. This was neither 766 mg purified anthocyanins nor a universal optimum. Neutrophil measurements cannot be relabeled direct endothelial NOX inhibition. [Rodriguez-Mateos et al., 2013](https://pubmed.ncbi.nlm.nih.gov/24004888/).
Complete structured claim and evidence
Blueberry polyphenol intake increased FMD at 1-2 and 6 hours in the acute healthy-men crossover study.
Blueberry polyphenol drink in acute vascular studies → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Blueberry polyphenol drink", "comparator": "Macronutrient- and micronutrient-matched control drink", "endpoint": "Blueberry polyphenol intake increased FMD at 1-2 and 6 hours in the acute healthy-men crossover study.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
21 healthy men across acute time/intake studies; total-polyphenol plateau near 766 mg.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Dose is total polyphenols, not purified anthocyanins; no universal optimum or cardiovascular-event endpoint.
plain_language
Blueberry polyphenol intake increased FMD at 1-2 and 6 hours in the acute healthy-men crossover study.
primary_references
Intake and time dependence of blueberry flavonoid-induced improvements in vascular function: a randomized, controlled, double-blind, crossover intervention study with mechanistic insights into biological activity. | 2013 | DOI 10.3945/ajcn.113.066639 | PMID 24004888 | https://pubmed.ncbi.nlm.nih.gov/24004888/ | https://doi.org/10.3945/ajcn.113.066639
source_locator
Reviewed reference lines 54-54; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 54–54
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 21 healthy men across acute time/intake studies; total-polyphenol plateau near 766 mg. · Recorded from source · Recorded from source
**Blueberry FMD timing tracks a changing exposure.** Acute crossover experiments in healthy men found FMD increases at 1–2 and six hours, associated with circulating phenolics and lower neutrophil NADPH-oxidase activity. A plateau occurred above roughly 766 mg of total blueberry polyphenols in that protocol. This was neither 766 mg purified anthocyanins nor a universal optimum. Neutrophil measurements cannot be relabeled direct endothelial NOX inhibition. [Rodriguez-Mateos et al., 2013](https://pubmed.ncbi.nlm.nih.gov/24004888/).
Complete structured claim and evidence
Purified anthocyanins improved FMD in healthy humans in the 2019 experimental program.
Purified anthocyanin preparation in Rodriguez-Mateos 2019 → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Purified anthocyanin preparation", "comparator": "Control preparation", "endpoint": "Purified anthocyanins improved FMD in healthy humans in the 2019 experimental program.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human purified-anthocyanin comparison, distinct from blueberry, metabolite association and mouse-injection experiments.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact dose-series values not extracted from accessible abstract. Mouse metabolite dosing is not human mediation proof.
plain_language
Purified anthocyanins improved FMD in healthy humans in the 2019 experimental program.
primary_references
Circulating Anthocyanin Metabolites Mediate Vascular Benefits of Blueberries: Insights From Randomized Controlled Trials, Metabolomics, and Nutrigenomics. | 2019 | DOI 10.1093/gerona/glz047 | PMID 30772905 | https://pubmed.ncbi.nlm.nih.gov/30772905/ | https://doi.org/10.1093/gerona/glz047
source_locator
Reviewed reference lines 56-56; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 56–56
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human purified-anthocyanin comparison, distinct from blueberry, metabolite association and mouse-injection experiments. · Recorded from source · Recorded from source
**Metabolite-mediated vascular activity has been tested.** A 2019 program compared purified anthocyanins, blueberries and control preparations in people, related circulating metabolites to FMD, and tested selected metabolite administration in mice. Purified anthocyanins improved FMD, while fiber/mineral/vitamin control drinks did not show the same effect. Human associations, mouse interventions and blood-cell gene-expression changes are different evidence layers. They support further metabolite research; they do not prove every correlated molecule is necessary or sufficient in humans. [Rodriguez-Mateos et al., 2019](https://pubmed.ncbi.nlm.nih.gov/30772905/).
Complete structured claim and evidence
Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HUVEC under the tested conditions.
Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures → Soluble VCAM-1 release by human umbilical-vein endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF plus vehicle added · Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF plus vehicle present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G serum-signature mixture plus TNF", "comparator": "TNF plus vehicle", "endpoint": "Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HUVEC under the tested conditions.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "c3g-human-serum-metabolite-signatures", "state": "added"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HUVEC culture; 1/6/24-hour serum signatures; 0.1x/1x/10x observed mean concentrations; 24-hour cytokine stimulation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Some VCAM effects survived 0.19-0.44 uM total mixture; not every endpoint or every concentration. Mixture does not identify one active component.
plain_language
Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HUVEC under the tested conditions.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HUVEC culture; 1/6/24-hour serum signatures; 0.1x/1x/10x observed mean concentrations; 24-hour cytokine stimulation. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HCAEC under the tested conditions.
Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures → Soluble VCAM-1 release by human coronary-artery endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF plus vehicle added · Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF plus vehicle present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G serum-signature mixture plus TNF", "comparator": "TNF plus vehicle", "endpoint": "Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HCAEC under the tested conditions.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "c3g-human-serum-metabolite-signatures", "state": "added"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HCAEC culture; 1/6/24-hour serum signatures; 0.1x/1x/10x observed mean concentrations; 24-hour cytokine stimulation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Some VCAM effects survived 0.19-0.44 uM total mixture; not every endpoint or every concentration. Mixture does not identify one active component.
plain_language
Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HCAEC under the tested conditions.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HCAEC culture; 1/6/24-hour serum signatures; 0.1x/1x/10x observed mean concentrations; 24-hour cytokine stimulation. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
C3G metabolite mixtures reduced IL-6 secretion at selected concentrations in HUVECs.
Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures → IL-6 release by human umbilical-vein endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF plus vehicle added · Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF plus vehicle present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Metabolite signature plus TNF", "comparator": "TNF plus vehicle", "endpoint": "C3G metabolite mixtures reduced IL-6 secretion at selected concentrations in HUVECs.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "c3g-human-serum-metabolite-signatures", "state": "added"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HUVEC; Figure 3; 24-hour TNF challenge at 10 ng/mL.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The HUVEC effect was absent at the lowest mixture concentrations; HCAEC protein-release null remains separate from transcript results. Different cell types and TNF stimuli are not an unexplained literature conflict.
plain_language
C3G metabolite mixtures reduced IL-6 secretion at selected concentrations in HUVECs.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HUVEC; Figure 3; 24-hour TNF challenge at 10 ng/mL. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
C3G metabolite mixtures did not significantly reduce IL-6 secretion in HCAECs.
Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures → IL-6 release by human coronary-artery endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF plus vehicle added · Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF plus vehicle present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Metabolite signature plus TNF", "comparator": "TNF plus vehicle", "endpoint": "C3G metabolite mixtures did not significantly reduce IL-6 secretion in HCAECs.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "c3g-human-serum-metabolite-signatures", "state": "added"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HCAEC; Figure 3; 24-hour TNF challenge at 0.1 ng/mL.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The HUVEC effect was absent at the lowest mixture concentrations; HCAEC protein-release null remains separate from transcript results. Different cell types and TNF stimuli are not an unexplained literature conflict.
plain_language
C3G metabolite mixtures did not significantly reduce IL-6 secretion in HCAECs.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HCAEC; Figure 3; 24-hour TNF challenge at 0.1 ng/mL. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
The tested metabolite signatures did not significantly change phosphorylated NF-kappa-B p65 in stimulated HCAECs.
Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures → NF-kappa-B p65 phosphorylation in human coronary-artery endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF plus vehicle added · Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF plus vehicle present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G-derived metabolite signatures plus TNF", "comparator": "TNF plus vehicle", "endpoint": "The tested metabolite signatures did not significantly change phosphorylated NF-kappa-B p65 in stimulated HCAECs.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "c3g-human-serum-metabolite-signatures", "state": "added"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HCAEC, Figure 5; highest tested mixture concentrations, brief TNF-stimulated phosphorylation assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Phosphorylation endpoint at specified sampling, not proof of absent signaling at every time or in all cell types.
plain_language
The tested metabolite signatures did not significantly change phosphorylated NF-kappa-B p65 in stimulated HCAECs.
primary_references
Signatures of anthocyanin metabolites identified in humans inhibit biomarkers of vascular inflammation in human endothelial cells. | 2017 | DOI 10.1002/mnfr.201700053 | PMID 28457017 | https://pubmed.ncbi.nlm.nih.gov/28457017/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/ | https://doi.org/10.1002/mnfr.201700053
source_locator
Reviewed reference lines 58-58; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 58–58
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HCAEC, Figure 5; highest tested mixture concentrations, brief TNF-stimulated phosphorylation assay. · Recorded from source · Recorded from source
**Low-concentration mixtures can change VCAM-1 without a universal IL-6 effect.** Warner's 2017 study reconstructed the tracer cohort's 1-, 6- and 24-hour serum signatures. Mixtures reduced TNF-stimulated VCAM-1; some effects remained at total concentrations of 0.19–0.44 µM. IL-6 secretion decreased in HUVECs at selected higher mixture concentrations, but not detectably in HCAECs. TNF stimulation also differed between the cell types. Figure 3 preserves this important cell-specific null. Phosphorylated NF-κB p65 did not significantly change in the tested HCAEC experiment. These are mixture findings, not proof that PCA alone suppresses NF-κB at dietary exposure. [Warner et al., 2017, Figures 2–5](https://pmc.ncbi.nlm.nih.gov/articles/PMC5600085/).
Complete structured claim and evidence
One-cup-equivalent daily blueberry powder improved FMD in the six-month metabolic-syndrome trial.
Blueberry powder standardized to half- or one-cup equivalents in Curtis 2019 → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "One-cup-equivalent blueberry powder daily", "comparator": "Matched placebo for six months", "endpoint": "One-cup-equivalent daily blueberry powder improved FMD in the six-month metabolic-syndrome trial.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
115 completers; metabolic syndrome; six-month randomized trial; one-cup equivalent arm.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Whole-blueberry preparation, not isolated anthocyanins. Clinical event prevention was not measured; Table 2 insulin-unit corrigendum retained.
plain_language
One-cup-equivalent daily blueberry powder improved FMD in the six-month metabolic-syndrome trial.
primary_references
Blueberries improve biomarkers of cardiometabolic function in participants with metabolic syndrome-results from a 6-month, double-blind, randomized controlled trial. | 2019 | DOI 10.1093/ajcn/nqy380 | PMID 31136659 | https://pubmed.ncbi.nlm.nih.gov/31136659/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/ | https://doi.org/10.1093/ajcn/nqy380
source_locator
Reviewed reference lines 62-62; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 62–62
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 115 completers; metabolic syndrome; six-month randomized trial; one-cup equivalent arm. · Recorded from source · Recorded from source
**Clinical nulls remain part of the mechanism reference.** In 115 adults with metabolic syndrome completing a six-month randomized blueberry trial, one-cup-equivalent intake improved FMD, but insulin resistance, blood pressure, pulse-wave velocity, NO and overall plasma thiol status did not significantly improve. Half-cup-equivalent intake did not improve the reported biomarkers. These results do not contradict every short-term purified-compound study; they constrain extrapolation across preparations, durations and endpoints. [Curtis et al., 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/). Its corrigendum changes the insulin unit in Table 2 to mU/L; it does not announce a reversal of the trial's outcomes. [Publisher correction](https://pmc.ncbi.nlm.nih.gov/articles/PMC6821540/).
Complete structured claim and evidence
Insulin resistance did not significantly improve in the six-month blueberry trial.
Blueberry powder standardized to half- or one-cup equivalents in Curtis 2019 → HOMA-IR estimate of insulin resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Daily blueberry powder", "comparator": "Matched placebo", "endpoint": "Insulin resistance did not significantly improve in the six-month blueberry trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Adults with metabolic syndrome, six months; HOMA-IR primary endpoint.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not proof of universal absence of metabolic effects; preparation, population and duration constrain interpretation. Corrigendum concerns insulin units, not reversal of outcome.
plain_language
Insulin resistance did not significantly improve in the six-month blueberry trial.
primary_references
Blueberries improve biomarkers of cardiometabolic function in participants with metabolic syndrome-results from a 6-month, double-blind, randomized controlled trial. | 2019 | DOI 10.1093/ajcn/nqy380 | PMID 31136659 | https://pubmed.ncbi.nlm.nih.gov/31136659/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/ | https://doi.org/10.1093/ajcn/nqy380
source_locator
Reviewed reference lines 62-62; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 62–62
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Adults with metabolic syndrome, six months; HOMA-IR primary endpoint. · Recorded from source · Recorded from source
**Clinical nulls remain part of the mechanism reference.** In 115 adults with metabolic syndrome completing a six-month randomized blueberry trial, one-cup-equivalent intake improved FMD, but insulin resistance, blood pressure, pulse-wave velocity, NO and overall plasma thiol status did not significantly improve. Half-cup-equivalent intake did not improve the reported biomarkers. These results do not contradict every short-term purified-compound study; they constrain extrapolation across preparations, durations and endpoints. [Curtis et al., 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/). Its corrigendum changes the insulin unit in Table 2 to mU/L; it does not announce a reversal of the trial's outcomes. [Publisher correction](https://pmc.ncbi.nlm.nih.gov/articles/PMC6821540/).
Complete structured claim and evidence
Half-cup-equivalent blueberry intake did not improve FMD in the six-month trial.
Blueberry powder standardized to half- or one-cup equivalents in Curtis 2019 → Brachial artery flow-mediated dilation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Half-cup-equivalent blueberry powder daily", "comparator": "Matched placebo", "endpoint": "Half-cup-equivalent blueberry intake did not improve FMD in the six-month trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Metabolic syndrome; half-cup-equivalent arm; six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Does not establish a universal daily-dose threshold.
plain_language
Half-cup-equivalent blueberry intake did not improve FMD in the six-month trial.
primary_references
Blueberries improve biomarkers of cardiometabolic function in participants with metabolic syndrome-results from a 6-month, double-blind, randomized controlled trial. | 2019 | DOI 10.1093/ajcn/nqy380 | PMID 31136659 | https://pubmed.ncbi.nlm.nih.gov/31136659/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/ | https://doi.org/10.1093/ajcn/nqy380
source_locator
Reviewed reference lines 62-62; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 62–62
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Metabolic syndrome; half-cup-equivalent arm; six months. · Recorded from source · Recorded from source
**Clinical nulls remain part of the mechanism reference.** In 115 adults with metabolic syndrome completing a six-month randomized blueberry trial, one-cup-equivalent intake improved FMD, but insulin resistance, blood pressure, pulse-wave velocity, NO and overall plasma thiol status did not significantly improve. Half-cup-equivalent intake did not improve the reported biomarkers. These results do not contradict every short-term purified-compound study; they constrain extrapolation across preparations, durations and endpoints. [Curtis et al., 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6537945/). Its corrigendum changes the insulin unit in Table 2 to mU/L; it does not announce a reversal of the trial's outcomes. [Publisher correction](https://pmc.ncbi.nlm.nih.gov/articles/PMC6821540/).
Complete structured claim and evidence
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.
Human microRNA-10b → Human ATP-binding cassette transporter A1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
human-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Primary abstract identifies both species in functional analyses. Exact construct/dose/endpoint tables require full extraction. No direct PCA intervention is silently substituted for the miRNA experiment.
plain_language
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · human-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.
Human microRNA-10b → Human ATP-binding cassette transporter G1 / ABCG1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
human-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Primary abstract identifies both species in functional analyses. Exact construct/dose/endpoint tables require full extraction. No direct PCA intervention is silently substituted for the miRNA experiment.
plain_language
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · human-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
miR-10b negatively regulated cholesterol efflux in human-derived macrophage experiments.
Human microRNA-10b → Cholesterol efflux from human-derived macrophages Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
human-derived macrophage functional experiments.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Abstract-level species attribution. Context and dose unextracted; not clinical efficacy.
plain_language
miR-10b negatively regulated cholesterol efflux in human-derived macrophage experiments.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · human-derived macrophage functional experiments. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.
Mouse microRNA-10b → Mouse ATP-binding cassette transporter A1 / Abca1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
mouse-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Primary abstract identifies both species in functional analyses. Exact construct/dose/endpoint tables require full extraction. No direct PCA intervention is silently substituted for the miRNA experiment.
plain_language
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · mouse-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.
Mouse microRNA-10b → Mouse ATP-binding cassette transporter G1 / Abcg1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
mouse-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Primary abstract identifies both species in functional analyses. Exact construct/dose/endpoint tables require full extraction. No direct PCA intervention is silently substituted for the miRNA experiment.
plain_language
Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · mouse-derived macrophage functional experiments; detailed intervention magnitudes and timing unextracted. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
miR-10b negatively regulated cholesterol efflux in mouse-derived macrophage experiments.
Mouse microRNA-10b → Cholesterol efflux from mouse-derived macrophages Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
mouse-derived macrophage functional experiments.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Abstract-level species attribution. Context and dose unextracted; not clinical efficacy.
plain_language
miR-10b negatively regulated cholesterol efflux in mouse-derived macrophage experiments.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · mouse-derived macrophage functional experiments. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
PCA reduced macrophage miR-10b and increased ABCA1/ABCG1-related cholesterol efflux in the reported experimental program.
Protocatechuic acid / 3,4-dihydroxybenzoic acid → Macrophage miR-10b and ABCA1/ABCG1 response, species-specific PCA endpoints not fully extracted Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "PCA exposure", "comparator": "Matched macrophage assay control; C3G comparator also reported", "endpoint": "PCA reduced macrophage miR-10b and increased ABCA1/ABCG1-related cholesterol efflux in the reported experimental program.", "effect_direction": "mixed", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mixed mouse/human-derived macrophage program; exact species assignment of each PCA endpoint remains unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Do not treat all listed homologs as simultaneously measured PCA targets in one species. Full paper required for species-separated PCA edges and exact concentrations.
plain_language
PCA reduced macrophage miR-10b and increased ABCA1/ABCG1-related cholesterol efflux in the reported experimental program.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mixed mouse/human-derived macrophage program; exact species assignment of each PCA endpoint remains unextracted. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
C3G consumption promoted macrophage reverse cholesterol transport in the microbiota-dependent ApoE-deficient mouse setting.
Cyanidin 3-O-beta-D-glucopyranoside → Macrophage reverse cholesterol transport in mice Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "C3G feeding in mice with the relevant microbiota condition", "comparator": "Matched control feeding", "endpoint": "C3G consumption promoted macrophage reverse cholesterol transport in the microbiota-dependent ApoE-deficient mouse setting.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
ApoE-deficient mouse feeding experiment; antibiotics and microbiota reacquisition used to investigate dependence.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Diet dose/duration not extracted from accessible abstract. Antibiotics are not selective blockade of a single metabolic step; no human plaque regression inferred.
plain_language
C3G consumption promoted macrophage reverse cholesterol transport in the microbiota-dependent ApoE-deficient mouse setting.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · ApoE-deficient mouse feeding experiment; antibiotics and microbiota reacquisition used to investigate dependence. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
C3G consumption reduced atherosclerotic lesion burden in the microbiota-dependent ApoE-deficient mouse setting.
Cyanidin 3-O-beta-D-glucopyranoside → Mouse atherosclerotic lesion burden Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "C3G feeding in mice with the relevant microbiota condition", "comparator": "Matched control feeding", "endpoint": "C3G consumption reduced atherosclerotic lesion burden in the microbiota-dependent ApoE-deficient mouse setting.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
ApoE-deficient mouse feeding experiment; antibiotics and microbiota reacquisition used to investigate dependence.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Diet dose/duration not extracted from accessible abstract. Antibiotics are not selective blockade of a single metabolic step; no human plaque regression inferred.
plain_language
C3G consumption reduced atherosclerotic lesion burden in the microbiota-dependent ApoE-deficient mouse setting.
primary_references
Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. | 2012 | DOI 10.1161/circresaha.112.266502 | PMID 22821931 | https://pubmed.ncbi.nlm.nih.gov/22821931/ | https://doi.org/10.1161/circresaha.112.266502
source_locator
Reviewed reference lines 66-66; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 66–66
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · ApoE-deficient mouse feeding experiment; antibiotics and microbiota reacquisition used to investigate dependence. · Recorded from source · Recorded from source
**PCA–miR-10b–cholesterol export is a specific experimental branch.** In ApoE-deficient mice, antibiotic depletion and microbiota reacquisition supported microbial involvement in C3G-to-PCA metabolism. PCA reduced macrophage miR-10b; functional tests showed miR-10b repressing ABCA1 and ABCG1 and limiting cholesterol efflux. PCA, unlike C3G at the compared concentrations, increased transporter expression and efflux. C3G feeding promoted macrophage reverse cholesterol transport and lesion regression in the microbiota-dependent mouse setting. The accessible primary abstract reports human- and mouse-derived macrophage experiments but does not fully separate every endpoint by species or list all doses; those remain extraction limits. [Wang et al., 2012](https://pubmed.ncbi.nlm.nih.gov/22821931/).
Complete structured claim and evidence
In human omental adipocytes, 50 uM cyanidin-3-glucoside increased glucose uptake in the tested culture model.
Cyanidin 3-O-beta-D-glucopyranoside → Human adipocyte insulin-stimulated glucose uptake Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "50 uM cyanidin-3-glucoside", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 50 uM cyanidin-3-glucoside increased glucose uptake in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
plain_language
In human omental adipocytes, 50 uM cyanidin-3-glucoside increased glucose uptake in the tested culture model.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.
Cyanidin 3-O-beta-D-glucopyranoside → GLUT4 recruitment to human adipocyte plasma membrane Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "50 uM cyanidin-3-glucoside", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
plain_language
In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.
Cyanidin 3-O-beta-D-glucopyranoside → Mouse GLUT4 movement toward or into the cell surface Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
cyanidin-3-glucoside with functional mouse Pparg present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
cyanidin-3-glucoside with functional mouse Pparg inhibited or silenced · Mouse peroxisome proliferator-activated receptor gamma / Pparg Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "cyanidin-3-glucoside with mouse Pparg inhibition/silencing", "comparator": "cyanidin-3-glucoside with functional mouse Pparg", "endpoint": "PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "mouse-pparg", "state": "inhibited or silenced"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse 3T3-L1, Figure 7: mouse Pparg siRNA/scrambled comparison and GW9662 antagonist; 10 uM C3G or 100 uM PCA.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Mouse perturbation, not a human knockdown. Supports pathway involvement, not direct binding affinity or clinical supplementation efficacy.
plain_language
PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse 3T3-L1, Figure 7: mouse Pparg siRNA/scrambled comparison and GW9662 antagonist; 10 uM C3G or 100 uM PCA. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
In human omental adipocytes, 100 uM protocatechuic-acid increased glucose uptake in the tested culture model.
Protocatechuic acid / 3,4-dihydroxybenzoic acid → Human adipocyte insulin-stimulated glucose uptake Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "100 uM protocatechuic-acid", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 100 uM protocatechuic-acid increased glucose uptake in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
plain_language
In human omental adipocytes, 100 uM protocatechuic-acid increased glucose uptake in the tested culture model.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.
Protocatechuic acid / 3,4-dihydroxybenzoic acid → GLUT4 recruitment to human adipocyte plasma membrane Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "100 uM protocatechuic-acid", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
plain_language
In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.
Protocatechuic acid / 3,4-dihydroxybenzoic acid → Mouse GLUT4 movement toward or into the cell surface Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
protocatechuic-acid with functional mouse Pparg inhibited or silenced · Mouse peroxisome proliferator-activated receptor gamma / Pparg Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
protocatechuic-acid with functional mouse Pparg present · Protocatechuic acid / 3,4-dihydroxybenzoic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "protocatechuic-acid with mouse Pparg inhibition/silencing", "comparator": "protocatechuic-acid with functional mouse Pparg", "endpoint": "PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "protocatechuic-acid", "state": "present"}, {"entity_slug": "mouse-pparg", "state": "inhibited or silenced"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse 3T3-L1, Figure 7: mouse Pparg siRNA/scrambled comparison and GW9662 antagonist; 10 uM C3G or 100 uM PCA.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Mouse perturbation, not a human knockdown. Supports pathway involvement, not direct binding affinity or clinical supplementation efficacy.
plain_language
PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.
primary_references
Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
source_locator
Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse 3T3-L1, Figure 7: mouse Pparg siRNA/scrambled comparison and GW9662 antagonist; 10 uM C3G or 100 uM PCA. · Recorded from source · Recorded from source
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidence
C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.
Cyanidin 3-O-beta-D-glucopyranoside → IRS1/PI3K/Akt insulin-signaling readouts in human endothelium Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_condition
Palmitate challenge without C3G challenge · Palmitate / hexadecanoate Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Palmitate challenge without C3G present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Palmitate challenge without C3G signaling stimulus · Insulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G pretreatment followed by palmitate challenge", "comparator": "Palmitate challenge without C3G", "endpoint": "C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "palmitate", "state": "challenge"}, {"entity_slug": "insulin", "state": "signaling stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Context-specific signaling rescue; no claim of direct KEAP1 binding or dietary circulating-metabolite effect.
plain_language
C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.
primary_references
Cyanidin-3-O-glucoside ameliorates palmitate-induced insulin resistance by modulating IRS-1 phosphorylation and release of endothelial derived vasoactive factors. | 2017 | DOI 10.1016/j.bbalip.2016.12.008 | PMID 28011403 | https://pubmed.ncbi.nlm.nih.gov/28011403/ | https://doi.org/10.1016/j.bbalip.2016.12.008
source_locator
Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 72–72
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted. · Recorded from source · Recorded from source
**Nrf2 dependence has been tested, but is context-specific.** C3G pretreatment in palmitate-challenged human endothelial cells improved IRS-1/PI3K/Akt-related insulin signaling and restored eNOS expression and NO release. Nrf2 silencing impaired the protective response. This is stronger than merely observing an antioxidant-gene increase, but neither direct KEAP1 binding nor the same action of circulating conjugates follows. The source's exact exposure protocol must accompany any quantitative reuse; only its accessible abstract was extracted here. [Fratantonio et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28011403/).
Complete structured claim and evidence
C3G pretreatment improved NO release in palmitate-challenged human endothelial cells.
Cyanidin 3-O-beta-D-glucopyranoside → Nitric oxide release by human endothelial cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_condition
Palmitate challenge without C3G challenge · Palmitate / hexadecanoate Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Palmitate challenge without C3G present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Palmitate challenge without C3G signaling stimulus · Insulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G pretreatment followed by palmitate challenge", "comparator": "Palmitate challenge without C3G", "endpoint": "C3G pretreatment improved NO release in palmitate-challenged human endothelial cells.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "palmitate", "state": "challenge"}, {"entity_slug": "insulin", "state": "signaling stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Context-specific signaling rescue; no claim of direct KEAP1 binding or dietary circulating-metabolite effect.
plain_language
C3G pretreatment improved NO release in palmitate-challenged human endothelial cells.
primary_references
Cyanidin-3-O-glucoside ameliorates palmitate-induced insulin resistance by modulating IRS-1 phosphorylation and release of endothelial derived vasoactive factors. | 2017 | DOI 10.1016/j.bbalip.2016.12.008 | PMID 28011403 | https://pubmed.ncbi.nlm.nih.gov/28011403/ | https://doi.org/10.1016/j.bbalip.2016.12.008
source_locator
Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 72–72
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted. · Recorded from source · Recorded from source
**Nrf2 dependence has been tested, but is context-specific.** C3G pretreatment in palmitate-challenged human endothelial cells improved IRS-1/PI3K/Akt-related insulin signaling and restored eNOS expression and NO release. Nrf2 silencing impaired the protective response. This is stronger than merely observing an antioxidant-gene increase, but neither direct KEAP1 binding nor the same action of circulating conjugates follows. The source's exact exposure protocol must accompany any quantitative reuse; only its accessible abstract was extracted here. [Fratantonio et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28011403/).
Complete structured claim and evidence
Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.
Cyanidin 3-O-beta-D-glucopyranoside → IRS1/PI3K/Akt insulin-signaling readouts in human endothelium Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_condition
C3G/palmitate experiment with Nrf2 retained challenge · Palmitate / hexadecanoate Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
C3G/palmitate experiment with Nrf2 retained present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
C3G/palmitate experiment with Nrf2 retained signaling stimulus · Insulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
C3G/palmitate experiment with Nrf2 retained silenced · Human Nrf2 / NFE2L2 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "C3G/palmitate experiment with Nrf2 silencing", "comparator": "C3G/palmitate experiment with Nrf2 retained", "endpoint": "Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "nfe2l2", "state": "silenced"}, {"entity_slug": "palmitate", "state": "challenge"}, {"entity_slug": "insulin", "state": "signaling stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HUVECs with Nrf2 transcript silencing and palmitate challenge.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact experimental details remain abstract-level; no clinical cofactor-rescue claim.
plain_language
Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.
primary_references
Cyanidin-3-O-glucoside ameliorates palmitate-induced insulin resistance by modulating IRS-1 phosphorylation and release of endothelial derived vasoactive factors. | 2017 | DOI 10.1016/j.bbalip.2016.12.008 | PMID 28011403 | https://pubmed.ncbi.nlm.nih.gov/28011403/ | https://doi.org/10.1016/j.bbalip.2016.12.008
source_locator
Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 72–72
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HUVECs with Nrf2 transcript silencing and palmitate challenge. · Recorded from source · Recorded from source
**Nrf2 dependence has been tested, but is context-specific.** C3G pretreatment in palmitate-challenged human endothelial cells improved IRS-1/PI3K/Akt-related insulin signaling and restored eNOS expression and NO release. Nrf2 silencing impaired the protective response. This is stronger than merely observing an antioxidant-gene increase, but neither direct KEAP1 binding nor the same action of circulating conjugates follows. The source's exact exposure protocol must accompany any quantitative reuse; only its accessible abstract was extracted here. [Fratantonio et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28011403/).
Complete structured claim and evidence
cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
Cyanidin 3-O-beta-D-glucopyranoside → Human Caco-2 paracellular permeability and electrical resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF without test glucoside present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "cyanidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
plain_language
cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
Delphinidin 3-O-beta-D-glucopyranoside → Human Caco-2 paracellular permeability and electrical resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF without test glucoside present · Delphinidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "delphinidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "delphinidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
plain_language
delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
Malvidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF without test glucoside present · Malvidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "malvidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "malvidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
plain_language
malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
Peonidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF without test glucoside present · Peonidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "peonidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "peonidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
plain_language
peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
Petunidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF without test glucoside present · Petunidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "petunidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "petunidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
plain_language
petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.
Cyanidin 3-O-beta-D-glucopyranoside → Myosin light-chain phosphorylation in human Caco-2 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF alone present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF alone present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "cyanidin-3-glucoside plus TNF", "comparator": "TNF alone", "endpoint": "The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Pathway evidence in cultured intestinal epithelium, not systemic NF-kappa-B suppression.
plain_language
The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.
Delphinidin 3-O-beta-D-glucopyranoside → Myosin light-chain phosphorylation in human Caco-2 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
TNF alone present · Delphinidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TNF alone present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "delphinidin-3-glucoside plus TNF", "comparator": "TNF alone", "endpoint": "The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "delphinidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Pathway evidence in cultured intestinal epithelium, not systemic NF-kappa-B suppression.
plain_language
The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.
primary_references
Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
source_locator
Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied. · Recorded from source · Recorded from source
**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
Complete structured claim and evidence
delphinidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 4.11 uM.
Delphinidin → Saccharomyces cerevisiae alpha-glucosidase assay enzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Purified delphinidin concentration series", "comparator": "Assay without inhibitor", "endpoint": "delphinidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 4.11 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Yeast enzyme assay; not human sucrase-isomaltase or maltase. IC50 depends on substrate and conditions; docking is not a human-target validation.
plain_language
delphinidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 4.11 uM.
primary_references
Investigation of Anthocyanidins and Anthocyanins for Targeting α-Glucosidase in Diabetes Mellitus. | 2020 | DOI 10.3746/pnf.2020.25.3.263 | PMID 33083375 | https://pubmed.ncbi.nlm.nih.gov/33083375/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/ | https://doi.org/10.3746/pnf.2020.25.3.263
source_locator
Reviewed reference lines 80-80; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 80–80
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C. · Recorded from source · Recorded from source
**Enzyme identity changes the digestive-enzyme claim.** A purified-compound assay used yeast α-glucosidase and a synthetic substrate, not human sucrase-isomaltase. Delphinidin aglycone inhibited with an IC50 near 4.11 µM; cyanidin was about 17.01 µM. Delphinidin-3-glucoside was much weaker, around 364 µM, and its 3,5-diglucoside showed no detected inhibition in the tested range. These values establish structure-dependent assay behavior. They cannot be imported as human intestinal IC50 values or a clinical comparison with acarbose. Docking does not repair that species/substrate gap. [Promyos et al., 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
cyanidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 17.01 uM.
Cyanidin → Saccharomyces cerevisiae alpha-glucosidase assay enzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Purified cyanidin concentration series", "comparator": "Assay without inhibitor", "endpoint": "cyanidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 17.01 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Yeast enzyme assay; not human sucrase-isomaltase or maltase. IC50 depends on substrate and conditions; docking is not a human-target validation.
plain_language
cyanidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 17.01 uM.
primary_references
Investigation of Anthocyanidins and Anthocyanins for Targeting α-Glucosidase in Diabetes Mellitus. | 2020 | DOI 10.3746/pnf.2020.25.3.263 | PMID 33083375 | https://pubmed.ncbi.nlm.nih.gov/33083375/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/ | https://doi.org/10.3746/pnf.2020.25.3.263
source_locator
Reviewed reference lines 80-80; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 80–80
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C. · Recorded from source · Recorded from source
**Enzyme identity changes the digestive-enzyme claim.** A purified-compound assay used yeast α-glucosidase and a synthetic substrate, not human sucrase-isomaltase. Delphinidin aglycone inhibited with an IC50 near 4.11 µM; cyanidin was about 17.01 µM. Delphinidin-3-glucoside was much weaker, around 364 µM, and its 3,5-diglucoside showed no detected inhibition in the tested range. These values establish structure-dependent assay behavior. They cannot be imported as human intestinal IC50 values or a clinical comparison with acarbose. Docking does not repair that species/substrate gap. [Promyos et al., 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
delphinidin-3-glucoside inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 364 uM.
Delphinidin 3-O-beta-D-glucopyranoside → Saccharomyces cerevisiae alpha-glucosidase assay enzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Purified delphinidin-3-glucoside concentration series", "comparator": "Assay without inhibitor", "endpoint": "delphinidin-3-glucoside inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 364 uM.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Yeast enzyme assay; not human sucrase-isomaltase or maltase. IC50 depends on substrate and conditions; docking is not a human-target validation.
plain_language
delphinidin-3-glucoside inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 364 uM.
primary_references
Investigation of Anthocyanidins and Anthocyanins for Targeting α-Glucosidase in Diabetes Mellitus. | 2020 | DOI 10.3746/pnf.2020.25.3.263 | PMID 33083375 | https://pubmed.ncbi.nlm.nih.gov/33083375/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/ | https://doi.org/10.3746/pnf.2020.25.3.263
source_locator
Reviewed reference lines 80-80; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 80–80
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae alpha-glucosidase, pNPG substrate, pH 6, 37 C. · Recorded from source · Recorded from source
**Enzyme identity changes the digestive-enzyme claim.** A purified-compound assay used yeast α-glucosidase and a synthetic substrate, not human sucrase-isomaltase. Delphinidin aglycone inhibited with an IC50 near 4.11 µM; cyanidin was about 17.01 µM. Delphinidin-3-glucoside was much weaker, around 364 µM, and its 3,5-diglucoside showed no detected inhibition in the tested range. These values establish structure-dependent assay behavior. They cannot be imported as human intestinal IC50 values or a clinical comparison with acarbose. Docking does not repair that species/substrate gap. [Promyos et al., 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
Delphinidin 3,5-diglucoside showed no detected yeast alpha-glucosidase inhibition in the tested range.
Delphinidin 3,5-O-diglucoside / delphin → Saccharomyces cerevisiae alpha-glucosidase assay enzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_contrast
{"intervention": "Delphinidin 3,5-diglucoside concentration series", "comparator": "No inhibitor", "endpoint": "Delphinidin 3,5-diglucoside showed no detected yeast alpha-glucosidase inhibition in the tested range.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Yeast alpha-glucosidase synthetic-substrate assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Assay-specific null; not every digestive enzyme or unlimited concentrations.
plain_language
Delphinidin 3,5-diglucoside showed no detected yeast alpha-glucosidase inhibition in the tested range.
primary_references
Investigation of Anthocyanidins and Anthocyanins for Targeting α-Glucosidase in Diabetes Mellitus. | 2020 | DOI 10.3746/pnf.2020.25.3.263 | PMID 33083375 | https://pubmed.ncbi.nlm.nih.gov/33083375/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/ | https://doi.org/10.3746/pnf.2020.25.3.263
source_locator
Reviewed reference lines 80-80; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 80–80
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Yeast alpha-glucosidase synthetic-substrate assay. · Recorded from source · Recorded from source
**Enzyme identity changes the digestive-enzyme claim.** A purified-compound assay used yeast α-glucosidase and a synthetic substrate, not human sucrase-isomaltase. Delphinidin aglycone inhibited with an IC50 near 4.11 µM; cyanidin was about 17.01 µM. Delphinidin-3-glucoside was much weaker, around 364 µM, and its 3,5-diglucoside showed no detected inhibition in the tested range. These values establish structure-dependent assay behavior. They cannot be imported as human intestinal IC50 values or a clinical comparison with acarbose. Docking does not repair that species/substrate gap. [Promyos et al., 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7541926/).
Complete structured claim and evidence
Ascorbic acid accelerated cyanidin-3-galactoside color loss at pH 3 and 25 C; 1000 mg/L shortened the modeled color half-life to about 0.3 days.
L-Ascorbate → Cyanidin-3-galactoside formulation color loss Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
experimental_condition
Same pigment without added ascorbic acid added · L-Ascorbate Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same pigment without added ascorbic acid present · Cyanidin 3-O-beta-D-galactopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Cyanidin-3-galactoside with added ascorbic acid", "comparator": "Same pigment without added ascorbic acid", "endpoint": "Ascorbic acid accelerated cyanidin-3-galactoside color loss at pH 3 and 25 C; 1000 mg/L shortened the modeled color half-life to about 0.3 days.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "ascorbate", "state": "added"}, {"entity_slug": "cyanidin-3-galactoside", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free pH 3 citrate-buffer formulation stored in the dark at 25 C; 250-1000 mg/L ascorbic acid; five-day observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Formulation chemistry; modeled absorbance decay is not human pharmacokinetics, loss of all biological activity, or systemic vitamin depletion.
plain_language
Ascorbic acid accelerated cyanidin-3-galactoside color loss at pH 3 and 25 C; 1000 mg/L shortened the modeled color half-life to about 0.3 days.
primary_references
Investigating the Interaction of Ascorbic Acid with Anthocyanins and Pyranoanthocyanins. | 2018 | DOI 10.3390/molecules23040744 | PMID 29570649 | https://pubmed.ncbi.nlm.nih.gov/29570649/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6017693/ | https://doi.org/10.3390/molecules23040744
source_locator
Reviewed reference lines 86-86; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 86–86
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free pH 3 citrate-buffer formulation stored in the dark at 25 C; 250-1000 mg/L ascorbic acid; five-day observation. · Recorded from source · Recorded from source
**Vitamin C can accelerate pigment loss in a formulation.** At pH 3 and 25 °C, added ascorbic acid accelerated bleaching of cyanidin-3-galactoside and chokeberry pigments. At 1,000 mg/L ascorbic acid, the modeled cyanidin-3-galactoside color half-life fell from about 22.8 days to 0.3 days. A carboxypyrano derivative resisted bleaching better but still reacted. These are storage chemistry and chemical-identity findings, not evidence that eating berries with vitamin C is harmful or causes systemic vitamin depletion. Color retention and intact-molecule retention must also be distinguished. [Farr and Giusti, 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6017693/).
Complete structured claim and evidence
Purified cyanidin bound iron in the reported cell-free assays.
Cyanidin → Iron complexation in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin bound iron in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Purified cyanidin reduced iron in the reported cell-free assays.
Cyanidin → Iron reduction in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin reduced iron in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Purified cyanidin reduced copper in the reported cell-free assays.
Cyanidin → Copper reduction in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin reduced copper in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Purified cyanidin-3-glucoside bound iron in the reported cell-free assays.
Cyanidin 3-O-beta-D-glucopyranoside → Iron complexation in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin-3-glucoside bound iron in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Purified cyanidin-3-glucoside reduced iron in the reported cell-free assays.
Cyanidin 3-O-beta-D-glucopyranoside → Iron reduction in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin-3-glucoside reduced iron in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Purified cyanidin-3-glucoside reduced copper in the reported cell-free assays.
Cyanidin 3-O-beta-D-glucopyranoside → Copper reduction in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Binding or reduction, not human absorption, intracellular stripping or ferroptosis prevention. Exact assay metal pools and doses require full methods.
plain_language
Purified cyanidin-3-glucoside reduced copper in the reported cell-free assays.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free spectrophotometric metal assays; multiple pH and compound/metal ratios; exact series not extracted. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
The tested cyanidin compounds and elderberry preparations had low copper-chelating activity despite their metal-reducing reactions.
Cyanidin 3-O-beta-D-glucopyranoside → Copper complexation in cell-free chemical assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary article abstract read in indexed publisher/author-hosted result; publisher full text unavailable. Exact pH series and extract/metal ratios not extracted.
experimental_model
Cell-free standardized spectrophotometric comparisons.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Low is not zero. Does not establish a clinical copper-depleting effect; extract composition and pH matter.
plain_language
The tested cyanidin compounds and elderberry preparations had low copper-chelating activity despite their metal-reducing reactions.
primary_references
Fruit extracts of 10 varieties of elderberry (Sambucus nigra L.) interact differently with iron and copper | 2016 | DOI 10.1016/j.phytol.2016.10.025 | https://doi.org/10.1016/j.phytol.2016.10.025
source_locator
Reviewed reference lines 88-88; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 88–88
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free standardized spectrophotometric comparisons. · Recorded from source · Recorded from source
**Iron binding and metal reduction are different reactions.** Purified cyanidin, C3G and standardized elderberry extracts chelated iron and reduced iron and copper in cell-free assays; copper-chelating activity was relatively low. Extract behavior varied and was not completely explained by pigment concentration. Binding a metal, changing its oxidation state and reducing intestinal absorption are three different endpoints. This does not establish removal of intracellular metals or protection from ferroptosis in people. [Mladěnka et al., 2016](https://doi.org/10.1016/j.phytol.2016.10.025).
Complete structured claim and evidence
Intact blackcurrant anthocyanins were detected in rat and rabbit ocular tissues after the reported oral or injected exposures.
Blackcurrant anthocyanin preparation in Matsumoto 2006 → Intact anthocyanin detection in rat and rabbit ocular tissues Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_model
Rats: oral and intraperitoneal studies; rabbits: intravenous study. Not equivalent routes or human exposures.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No human retinal concentration or vitamin-A replacement inferred. Route-specific doses not extracted from accessible abstract.
plain_language
Intact blackcurrant anthocyanins were detected in rat and rabbit ocular tissues after the reported oral or injected exposures.
primary_references
Comparative assessment of distribution of blackcurrant anthocyanins in rabbit and rat ocular tissues. | 2006 | DOI 10.1016/j.exer.2005.12.019 | PMID 16635490 | https://pubmed.ncbi.nlm.nih.gov/16635490/ | https://doi.org/10.1016/j.exer.2005.12.019
source_locator
Reviewed reference lines 96-96; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 96–96
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rats: oral and intraperitoneal studies; rabbits: intravenous study. Not equivalent routes or human exposures. · Recorded from source · Recorded from source
**Animal ocular delivery has been observed.** Blackcurrant anthocyanins were detected intact in rat and rabbit ocular tissues after the reported oral and injected administrations. Route and species matter: these experiments cannot establish a human retinal concentration after eating berries, an equivalence to vitamin A, or enhanced rhodopsin regeneration in people. [Matsumoto et al., 2006](https://pubmed.ncbi.nlm.nih.gov/16635490/).
Complete structured claim and evidence
Bilberry extract did not improve night visual acuity in the controlled healthy-young-men crossover trial.
Bilberry extract with 25% anthocyanosides in Muth 2000 → Human night visual acuity Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Bilberry extract for 21 days", "comparator": "Placebo in crossover", "endpoint": "Bilberry extract did not improve night visual acuity in the controlled healthy-young-men crossover trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
15 men, 160 mg 25%-anthocyanoside bilberry extract three times daily, 21 days, washout/crossover.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Specific preparation and healthy population; not all eye diseases or all anthocyanin structures.
plain_language
Bilberry extract did not improve night visual acuity in the controlled healthy-young-men crossover trial.
primary_references
The effect of bilberry nutritional supplementation on night visual acuity and contrast sensitivity. | 2000 | PMID 10767671 | https://pubmed.ncbi.nlm.nih.gov/10767671/
source_locator
Reviewed reference lines 98-98; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 98–98
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 15 men, 160 mg 25%-anthocyanoside bilberry extract three times daily, 21 days, washout/crossover. · Recorded from source · Recorded from source
**Controlled human night-vision results were negative.** A 15-man crossover trial used 160 mg bilberry extract containing 25% anthocyanosides three times daily for 21 days, with a washout and crossover. Night visual acuity and contrast sensitivity did not improve versus placebo. This constrains that preparation in healthy young men; it is not a finding about all eye diseases. Wartime anecdotes are not substitutes for this comparison. [Muth et al., 2000](https://pubmed.ncbi.nlm.nih.gov/10767671/).
Complete structured claim and evidence
Bilberry extract did not improve night contrast sensitivity in the controlled healthy-young-men crossover trial.
Bilberry extract with 25% anthocyanosides in Muth 2000 → Human night contrast sensitivity Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
experimental_contrast
{"intervention": "Bilberry extract for 21 days", "comparator": "Placebo in crossover", "endpoint": "Bilberry extract did not improve night contrast sensitivity in the controlled healthy-young-men crossover trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
15 men, 160 mg 25%-anthocyanoside bilberry extract three times daily, 21 days, washout/crossover.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Specific preparation and healthy population; not all eye diseases or all anthocyanin structures.
plain_language
Bilberry extract did not improve night contrast sensitivity in the controlled healthy-young-men crossover trial.
primary_references
The effect of bilberry nutritional supplementation on night visual acuity and contrast sensitivity. | 2000 | PMID 10767671 | https://pubmed.ncbi.nlm.nih.gov/10767671/
source_locator
Reviewed reference lines 98-98; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 98–98
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 15 men, 160 mg 25%-anthocyanoside bilberry extract three times daily, 21 days, washout/crossover. · Recorded from source · Recorded from source
**Controlled human night-vision results were negative.** A 15-man crossover trial used 160 mg bilberry extract containing 25% anthocyanosides three times daily for 21 days, with a washout and crossover. Night visual acuity and contrast sensitivity did not improve versus placebo. This constrains that preparation in healthy young men; it is not a finding about all eye diseases. Wartime anecdotes are not substitutes for this comparison. [Muth et al., 2000](https://pubmed.ncbi.nlm.nih.gov/10767671/).
Complete structured claim and evidence

Availability and dependencies

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

SGLT1 or GLUT2 knockdown limits tested C3G transport

Condition: machinery_impairment · Separate SLC5A1 or SLC2A2 siRNA knockdown, compared with scrambled siRNA.

Normal role: Intact carrier machinery contributes to transport of C3G in the tested monolayers.

Recorded consequence: Reduced C3G transport under the matched exposure.

Scope: Specific compound and model named above; grouped for navigation under the anthocyanin chapter.

Mouse PPARgamma disruption blocks tested C3G/PCA adipocyte responses

Condition: machinery_impairment · Mouse Pparg siRNA or the antagonist GW9662 during separate compound exposures.

Normal role: The tested C3G or PCA exposures recruit GLUT4 with functional Pparg.

Recorded consequence: Loss of the reported GLUT4 recruitment and target-gene response.

Scope: Specific compound and model named above; grouped for navigation under the anthocyanin chapter.

Nrf2 silencing limits C3G-associated endothelial protection

Condition: machinery_impairment · Silencing NFE2L2 during the C3G/palmitate experiment.

Normal role: C3G pretreatment improves the reported insulin-signaling response under the specified challenge.

Recorded consequence: Impaired C3G-associated protective response.

Scope: Specific compound and model named above; grouped for navigation under the anthocyanin chapter.

The sources

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

Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026)Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · Recorded from sourceRead preserved source

Recorded disagreements

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

Open questions in this collection

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

1. **Which circulating components are necessary?** Reconstruct measured time-dependent mixtures and perform removal/add-back comparisons. Do effects survive removal of PCA, its conjugates, or other components at observed exposures?Open research question from the reviewed reference; not an established causal claim.
2. **Why do endothelial beds differ?** Can the HUVEC/HCAEC IL-6 difference be reproduced under matched TNF stimulus, exposure, sampling time and assay sensitivity? Measure protein release separately from transcription.Open research question from the reviewed reference; not an established causal claim.
3. **What reaches the transporters in a meal?** How do glucose, glycoside structure, luminal pH and food matrix change SGLT1/GLUT2-associated anthocyanin transport without disrupting epithelial integrity?Open research question from the reviewed reference; not an established causal claim.
4. **When does the cholesterol branch work?** Does exposure-matched PCA change miR-10b and ABCA1/ABCG1-dependent efflux in human macrophages with defined cholesterol acceptors? Does it persist when transporter expression, ATP supply or acceptor availability becomes limiting?Open research question from the reviewed reference; not an established causal claim.
5. **Can a signaling response survive cofactor limitation?** In endothelial cells, which resource limitations prevent an anthocyanin/metabolite mixture from changing NO output despite a signaling response? Test the limiting resource directly rather than inferring synergy from a shared enzyme.Open research question from the reviewed reference; not an established causal claim.
6. **What does vitamin C change before ingestion?** Does formulation storage alter the actual anthocyanin species delivered, and does the changed chemical profile alter intestinal versus circulating exposure?Open research question from the reviewed reference; not an established causal claim.
7. **When does iron binding change absorption?** Compare defined pigments, molar ratios, iron forms and ascorbate in a relevant meal model, then test human absorption. Chelation and reduction may push different steps in different directions.Open research question from the reviewed reference; not an established causal claim.
8. **Which chemical form drives barrier effects?** Compare intact glycosides, conjugates and measured degradation mixtures with electrical resistance, solute flux and pathway interventions together.Open research question from the reviewed reference; not an established causal claim.
9. **How far does microbial attribution extend?** Use labeled substrates and selective interventions to distinguish microbial conversion from chemical breakdown and shared dietary sources; broad antibiotics cannot isolate every step.Open research question from the reviewed reference; not an established causal claim.
10. **Which clinical response is reproducible?** Independently validate exposure-response predictors and retain null endpoints. Parent disappearance, a graph route and a statistically associated metabolite each leave a different causal gap.Open research question from the reviewed reference; not an established causal claim.

Chapters contain source-recorded findings and curated literature summaries. Read each finding's evidence grade, experimental context and review qualifications. The ledger is not medical advice.

Anthocyanins

The mechanisms

The anthocyanin class includes Cyanidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.

The anthocyanin class includes Cyanidin 3-O-beta-D-galactopyranoside; membership does not transfer experimental effects.

The anthocyanin class includes Cyanidin 3,5-O-diglucoside / cyanin; membership does not transfer experimental effects.

The anthocyanin class includes Delphinidin 3-O-beta-D-glucopyranoside; membership does not transfer experimental effects.

The anthocyanin class includes Malvidin 3-O-glucoside; membership does not transfer experimental effects.

The anthocyanin class includes Peonidin 3-O-glucoside; membership does not transfer experimental effects.

The anthocyanin class includes Petunidin 3-O-glucoside; membership does not transfer experimental effects.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The specified preparation contains anthocyanins; its experimental effects remain attached to the actual preparation.

The tested signatures reconstruct serum metabolite profiles measured after labeled C3G exposure; they are separate mixtures, not intact C3G.

Solution pH changes reversible molecular-form transitions of the tested anthocyanin glucosides; degradation is a separate process.

Anthocyanin structure changes parent stability during DMEM incubation at pH 7.4, 37 C and 5% CO2.

After 500 mg labeled C3G in eight men, urine plus breath contained 12.38% of administered label over 48 hours; this is not intact C3G recovery.

The tracer cohort had mean serum C3G Cmax 141 +/- 70 nM at 1.8 +/- 0.2 hours, measurable in five participants.

Labeled C3G produced circulating labeled PCA in humans; mean free PCA Cmax was 146 +/- 74 nM, n=8.

After labeled C3G ingestion, Protocatechuic-acid sulfate isomers, unresolved assay sum was detected as a labeled serum product with its own concentration-time profile.

After labeled C3G ingestion, Vanillic acid / 4-hydroxy-3-methoxybenzoic acid was detected as a labeled serum product with its own concentration-time profile.

After labeled C3G ingestion, Ferulic acid / 4-hydroxy-3-methoxycinnamic acid was detected as a labeled serum product with its own concentration-time profile.

After labeled C3G ingestion, Hippuric acid / benzoylglycine was detected as a labeled serum product with its own concentration-time profile.

After the tested blueberry meal, parent anthocyanins peaked earlier than several glucuronides and phenolic products.

Knocking down SLC5A1 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.

Knocking down SLC2A2 reduced C3G transport in differentiated human Caco-2 monolayers relative to scrambled siRNA.

The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.

The tested cyanidin glycoside reduced fluorescent glucose-analogue uptake in Caco-2 BBe1 cells at 50 uM.

The tested anthocyanin structures competed in a bilitranslocase transport assay; the class result was 17 of 20 compounds, Ki 1.4-22 uM.

Human fecal microbiota degraded the tested anthocyanins in anaerobic incubations, producing B-ring phenolic acids.

Separate rat microsomal experiments glucuronidated anthocyanins when activated glucuronic acid was supplied.

The tested NADPH-supported rat microsomal P450 system did not detect anthocyanin hydroxylation or demethylation.

The 12-week purified berry anthocyanin trial reported higher brachial FMD versus placebo.

The 12-week purified berry anthocyanin trial reported higher plasma cGMP versus placebo.

The 12-week purified berry anthocyanin trial reported lower circulating soluble VCAM-1 versus placebo.

NO-cGMP inhibitor interventions abolished the reported anthocyanin-associated endothelial response in a small human experiment.

Acute blueberry polyphenol intake was associated with lower neutrophil NADPH oxidase activity at times of improved FMD.

Blueberry polyphenol intake increased FMD at 1-2 and 6 hours in the acute healthy-men crossover study.

Purified anthocyanins improved FMD in healthy humans in the 2019 experimental program.

Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HUVEC under the tested conditions.

Reconstructed C3G metabolite mixtures lowered TNF-stimulated VCAM-1 release in HCAEC under the tested conditions.

C3G metabolite mixtures reduced IL-6 secretion at selected concentrations in HUVECs.

C3G metabolite mixtures did not significantly reduce IL-6 secretion in HCAECs.

The tested metabolite signatures did not significantly change phosphorylated NF-kappa-B p65 in stimulated HCAECs.

One-cup-equivalent daily blueberry powder improved FMD in the six-month metabolic-syndrome trial.

Insulin resistance did not significantly improve in the six-month blueberry trial.

Half-cup-equivalent blueberry intake did not improve FMD in the six-month trial.

Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.

Functional experiments reported that miR-10b represses ABCA1/ABCG1 in human-derived macrophages.

miR-10b negatively regulated cholesterol efflux in human-derived macrophage experiments.

Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.

Functional experiments reported that miR-10b represses ABCA1/ABCG1 in mouse-derived macrophages.

miR-10b negatively regulated cholesterol efflux in mouse-derived macrophage experiments.

PCA reduced macrophage miR-10b and increased ABCA1/ABCG1-related cholesterol efflux in the reported experimental program.

C3G consumption promoted macrophage reverse cholesterol transport in the microbiota-dependent ApoE-deficient mouse setting.

C3G consumption reduced atherosclerotic lesion burden in the microbiota-dependent ApoE-deficient mouse setting.

In human omental adipocytes, 50 uM cyanidin-3-glucoside increased glucose uptake in the tested culture model.

In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.

PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.

In human omental adipocytes, 100 uM protocatechuic-acid increased glucose uptake in the tested culture model.

In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.

PPARgamma inhibition or silencing blocked the polyphenol-associated GLUT4 recruitment in mouse 3T3-L1 adipocytes.

C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.

C3G pretreatment improved NO release in palmitate-challenged human endothelial cells.

Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.

cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.

delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.

malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.

The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.

delphinidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 4.11 uM.

cyanidin inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 17.01 uM.

delphinidin-3-glucoside inhibited yeast alpha-glucosidase in the synthetic-substrate assay; IC50 approximately 364 uM.

Delphinidin 3,5-diglucoside showed no detected yeast alpha-glucosidase inhibition in the tested range.

Ascorbic acid accelerated cyanidin-3-galactoside color loss at pH 3 and 25 C; 1000 mg/L shortened the modeled color half-life to about 0.3 days.