Component
NF-kappa-B p65 phosphorylation in human coronary-artery endothelial cells
NF-kappa-B p65 phosphorylation in human coronary-artery endothelial cells. Interpret through the linked experimental species, preparation, compartment and exposure; no universal causal effect is implied.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
The tested metabolite signatures did not significantly change phosphorylated NF-kappa-B p65 in stimulated HCAECs.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.