Component

Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures

Reconstructed 1-, 6- and 24-hour human C3G metabolite signatures. Interpret through the linked experimental species, preparation, compartment and exposure; no universal causal effect is implied.

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

  2. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

  3. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

  4. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

  5. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

What acts on it

  1. 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 source_derived_draftungraded
    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. · source_derived_draft · unverified_draft

    **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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.