Component

Human interleukin-1 alpha / IL1A

3 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. IL-1 alpha and IL-1 beta increased secretion of biologically active thymulin from cultured human TECs.

    Human interleukin-1 alpha / IL1A → Thymulin Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary bibliographic record and abstract checked; full methods/figures not comprehensively reviewed.
    experimental_contrast
    {"intervention": "IL-1 exposure", "comparator": "Untreated cultures", "endpoint": "IL-1 alpha and IL-1 beta increased secretion of biologically active thymulin from cultured human TECs.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Cultured human TECs; bioactivity readout, not native precursor-gene discovery.
    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
    IL-1 alpha and IL-1 beta increased secretion of biologically active thymulin from cultured human TECs.
    primary_references
    Interleukin 1 regulates secretion of zinc-thymulin by human thymic epithelial cells and its action on T-lymphocyte proliferation and nuclear protein kinase C. | 1992 | DOI 10.1073/pnas.89.16.7752 | PMID 1502195 | https://doi.org/10.1073/pnas.89.16.7752
    source_locator
    Reviewed reference lines 35-35; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 35–35

    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 · Cultured human TECs; bioactivity readout, not native precursor-gene discovery. · Recorded from source · Recorded from source

    In cultured human TECs, **IL-1α and IL-1β increased zinc uptake, metallothionein mRNA and secretion of biologically active thymulin**. Part of the IL-1 effect on zinc uptake occurred independently of proliferation. Metallothionein was proposed as an intracellular zinc donor; direct transfer from a defined metallothionein molecule to FTS was not resolved by these observations. Do not turn that proposal into an established transfer reaction. [Coto et al., 1992](https://doi.org/10.1073/pnas.89.16.7752)
    Complete structured claim and evidence

  2. IL-1 alpha and IL-1 beta increased zinc uptake in cultured human thymic epithelial cells; part of the response was independent of proliferation.

    Human interleukin-1 alpha / IL1A → Cellular zinc influx Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary bibliographic record and abstract checked; full methods/figures not comprehensively reviewed.
    experimental_contrast
    {"intervention": "IL-1 exposure", "comparator": "Untreated cultures", "endpoint": "IL-1 alpha and IL-1 beta increased zinc uptake in cultured human thymic epithelial cells; part of the response was independent of proliferation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Cultured human TECs; IL-1 exposure, uptake assay.
    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
    IL-1 alpha and IL-1 beta increased zinc uptake in cultured human thymic epithelial cells; part of the response was independent of proliferation.
    primary_references
    Interleukin 1 regulates secretion of zinc-thymulin by human thymic epithelial cells and its action on T-lymphocyte proliferation and nuclear protein kinase C. | 1992 | DOI 10.1073/pnas.89.16.7752 | PMID 1502195 | https://doi.org/10.1073/pnas.89.16.7752
    source_locator
    Reviewed reference lines 35-35; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 35–35

    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 · Cultured human TECs; IL-1 exposure, uptake assay. · Recorded from source · Recorded from source

    In cultured human TECs, **IL-1α and IL-1β increased zinc uptake, metallothionein mRNA and secretion of biologically active thymulin**. Part of the IL-1 effect on zinc uptake occurred independently of proliferation. Metallothionein was proposed as an intracellular zinc donor; direct transfer from a defined metallothionein molecule to FTS was not resolved by these observations. Do not turn that proposal into an established transfer reaction. [Coto et al., 1992](https://doi.org/10.1073/pnas.89.16.7752)
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.

    Apigenin → Senescence-associated secretory phenotype in apigenin-treated human fibroblasts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    experimental_contrast
    {"intervention": "Apigenin in senescent fibroblasts", "comparator": "Senescent vehicle controls", "endpoint": "Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.
    primary_references
    Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1
    source_locator
    Reviewed reference api-sasp; Primary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 752–758

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments. · Recorded from source · Recorded from source

    ### api-sasp Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers. Primary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis. Model and exposure: Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    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.