Component

Naringenin response in oxidatively stressed endothelial cells

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. SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury.

    Experimental context and source evidence
    dose
    Naringenin with SIRT1 siRNA
    duration
    Cell experiment accompanying three-month mouse dosing
    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
    Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm
    limitations
    SIRT1 involvement in a cell model does not establish direct SIRT1 binding or human atherosclerosis treatment.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm
    plain_language
    SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury.
    primary_references
    Naringenin ameliorates vascular senescence and atherosclerosis involving SIRT1 activation. (2023). https://pubmed.ncbi.nlm.nih.gov/37343148/ DOI: 10.1093/jpp/rgad053
    route
    In vitro perturbation
    tissue
    SIRT1, FOXO3a/PGC1alpha and senescence measures

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 143–152

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm · source_derived_draft · unverified_draft

    ## naringenin-sirt1-silencing SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury. Model/species: Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm Tissue/system: SIRT1, FOXO3a/PGC1alpha and senescence measures Exposure: Naringenin with SIRT1 siRNA Route: In vitro perturbation Duration: Cell experiment accompanying three-month mouse dosing Limits: SIRT1 involvement in a cell model does not establish direct SIRT1 binding or human atherosclerosis treatment. Primary reference: Naringenin ameliorates vascular senescence and atherosclerosis involving SIRT1 activation. (2023). https://pubmed.ncbi.nlm.nih.gov/37343148/ DOI: 10.1093/jpp/rgad053 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