Component

Human thyrotropin receptor / TSHR

Human thyrotropin receptor / TSHR

2 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. RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.

    Experimental context and source evidence
    evidence_access
    Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    experimental_contrast
    {"intervention": "Auto-oxidized RA with bovine TSH", "comparator": "Hormone without oxidized compound", "endpoint": "RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    1985 cell-free hormone-binding study; oxidation-product mixtures.
    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
    Rosmarinic acid collection; exact intervention and molecular form govern interpretation. · Rosmarinic acid
    plain_language
    RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.
    primary_references
    The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677
    source_locator
    Reviewed reference ra-thyroid-oxidized; Across eight active compounds, half-inhibition required products equivalent to 20–80 micrograms/mL starting compound. No RA-specific universal clinical threshold.

    Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 494–500

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 1985 cell-free hormone-binding study; oxidation-product mixtures. · Recorded from source · Recorded from source

    ### ra-thyroid-oxidized RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes. Across eight active compounds, half-inhibition required products equivalent to 20–80 micrograms/mL starting compound. No RA-specific universal clinical threshold. Model and exposure: 1985 cell-free hormone-binding study; oxidation-product mixtures. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | 1985 | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    Complete structured claim and evidence
  2. Unoxidized RA was inactive in the reported TSH-binding assay; activity emerged after auto-oxidation.

    Rosmarinic acid → Human thyrotropin receptor / TSHR 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": "Unoxidized compound", "comparator": "No compound", "endpoint": "Unoxidized RA was inactive in the reported TSH-binding assay; activity emerged after auto-oxidation.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    Same study; bovine TSH and human thyroid membranes.
    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
    Rosmarinic acid collection; exact intervention and molecular form govern interpretation. · Rosmarinic acid
    plain_language
    Unoxidized RA was inactive in the reported TSH-binding assay; activity emerged after auto-oxidation.
    primary_references
    The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677
    source_locator
    Reviewed reference ra-thyroid-unoxidized-null; The oxidation state is part of the experimental actor.

    Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 502–508

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Same study; bovine TSH and human thyroid membranes. · Recorded from source · Recorded from source

    ### ra-thyroid-unoxidized-null Unoxidized RA was inactive in the reported TSH-binding assay; activity emerged after auto-oxidation. The oxidation state is part of the experimental actor. Model and exposure: Same study; bovine TSH and human thyroid membranes. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | 1985 | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677 | 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.