Component

Human platelet cPLA2-to-NF-kappaB signaling axis

Species, preparation, dose and limitations are retained on linked claims.

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.

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 acts on it

  1. Eugenol reduced collagen-stimulated IKK and p65 phosphorylation and I-kappaB-alpha degradation; inhibitor ordering placed cPLA2 upstream of NF-kappaB in human platelets.

    Experimental context and source evidence
    dose
    Eugenol with CAY10502 or BAY11-7082 pathway probes
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Platelets from healthy human donors; mouse mesenteric-thrombosis arm
    limitations
    Anucleate platelet NF-kappaB signaling and mouse plug formation do not establish chronic human outcomes.
    nutrient_topic
    Eugenol chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Eugenol
    organism
    Platelets from healthy human donors; mouse mesenteric-thrombosis arm
    plain_language
    Eugenol reduced collagen-stimulated IKK and p65 phosphorylation and I-kappaB-alpha degradation; inhibitor ordering placed cPLA2 upstream of NF-kappaB in human platelets.
    primary_references
    Eugenol: A Potential Modulator of Human Platelet Activation and Mouse Mesenteric Vascular Thrombosis via an Innovative cPLA2-NF-κB Signaling Axis. (2024). https://pubmed.ncbi.nlm.nih.gov/39200154/ DOI: 10.3390/biomedicines12081689
    route
    In vitro and in vivo mouse model
    tissue
    cPLA2 and NF-kappaB signaling

    Eugenol: mechanism of action and interactions (2026-09-20) · lines 33–42

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Platelets from healthy human donors; mouse mesenteric-thrombosis arm · source_derived_draft · unverified_draft

    ## eugenol-cpla2-nfkb Eugenol reduced collagen-stimulated IKK and p65 phosphorylation and I-kappaB-alpha degradation; inhibitor ordering placed cPLA2 upstream of NF-kappaB in human platelets. Model/species: Platelets from healthy human donors; mouse mesenteric-thrombosis arm Tissue/system: cPLA2 and NF-kappaB signaling Exposure: Eugenol with CAY10502 or BAY11-7082 pathway probes Route: In vitro and in vivo mouse model Duration: Acute Limits: Anucleate platelet NF-kappaB signaling and mouse plug formation do not establish chronic human outcomes. Primary reference: Eugenol: A Potential Modulator of Human Platelet Activation and Mouse Mesenteric Vascular Thrombosis via an Innovative cPLA2-NF-κB Signaling Axis. (2024). https://pubmed.ncbi.nlm.nih.gov/39200154/ DOI: 10.3390/biomedicines12081689 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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.

    Evidence, AI assistance and curation standards