Component

Human platelet aggregation, agonist specified

Context-specific entity; species, compartment and exposure are stated on each claim.

5 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 acts on it

  1. Bromelain fractions II and III had both proteolytic and platelet-aggregation-inhibitory activity, and oxidation with sodium tetrathionate abolished both activities.

    Bromelain → Human platelet aggregation, agonist specified source_derived_draftungraded
    Experimental context and source evidence
    dose
    Purified bromelain fractions with or without oxidation
    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
    Fractionated commercial bromelain and platelet assays
    limitations
    The experiment links activities but did not identify the platelet substrate or establish an oral antithrombotic dose.
    nutrient_topic
    Bromelain chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Bromelain
    organism
    Fractionated commercial bromelain and platelet assays
    plain_language
    Bromelain fractions II and III had both proteolytic and platelet-aggregation-inhibitory activity, and oxidation with sodium tetrathionate abolished both activities.
    primary_references
    Chromatographic fractionation and characterization of the active platelet aggregation inhibitory factor from bromelain. (1979). https://pubmed.ncbi.nlm.nih.gov/485732/
    route
    In vitro
    tissue
    Protease activity and platelet aggregation

    Bromelain: mechanism of action and interactions (2026-09-20) · lines 121–130

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Fractionated commercial bromelain and platelet assays · source_derived_draft · unverified_draft

    ## bromelain-protease-platelet-link Bromelain fractions II and III had both proteolytic and platelet-aggregation-inhibitory activity, and oxidation with sodium tetrathionate abolished both activities. Model/species: Fractionated commercial bromelain and platelet assays Tissue/system: Protease activity and platelet aggregation Exposure: Purified bromelain fractions with or without oxidation Route: In vitro Duration: Acute Limits: The experiment links activities but did not identify the platelet substrate or establish an oral antithrombotic dose. Primary reference: Chromatographic fractionation and characterization of the active platelet aggregation inhibitory factor from bromelain. (1979). https://pubmed.ncbi.nlm.nih.gov/485732/ Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Inhibition of aggregation was not due to direct toxicity of these agents towards platelets as judged by LDH release, and the TRPV1 antagonist SB-452533 did not affect inhibition of ADP-induced platelet aggregation by capsaicin and N-oleoyldopamine.

    Dihydrocapsaicin → Human platelet aggregation, agonist specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/24953906.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717", "start_char": 0, "end_char": 1870, "text_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717"}
    experimental_model
    In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control
    exposure
    Capsaicin and dihydrocapsaicin against the endogenous vanilloids N-oleoyldopamine and N-arachidonoyl-dopamine, with ADP, collagen and arachidonic acid as agonists
    limitations
    The agonist-by-agonist design is what makes this useful: it separates the two plant compounds where a single-agonist study would have merged them. A TRPV1 antagonist control was included.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Human
    plain_language
    The platelets were not simply being killed, and again the receptor is not the route.
    primary_references
    [dhc-p24953906] Vanilloid-like agents inhibit aggregation of human platelets. (2014). https://pubmed.ncbi.nlm.nih.gov/24953906/ DOI: 10.1016/j.thromres.2014.05.038
    tissue_or_cell_type
    Platelets

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 166–177

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control · source_derived_draft · unverified_draft

    ### dhc-platelet-effect-not-trpv1 Inhibition of aggregation was not due to direct toxicity of these agents towards platelets as judged by LDH release, and the TRPV1 antagonist SB-452533 did not affect inhibition of ADP-induced platelet aggregation by capsaicin and N-oleoyldopamine. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The platelets were not simply being killed, and again the receptor is not the route. organism: Human tissue_or_cell_type: Platelets experimental_model: In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control limitations: The agonist-by-agonist design is what makes this useful: it separates the two plant compounds where a single-agonist study would have merged them. A TRPV1 antagonist control was included. exposure: Capsaicin and dihydrocapsaicin against the endogenous vanilloids N-oleoyldopamine and N-arachidonoyl-dopamine, with ADP, collagen and arachidonic acid as agonists evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24953906.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717", "start_char": 0, "end_char": 1870, "text_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717"} [dhc-p24953906] Vanilloid-like agents inhibit aggregation of human platelets. (2014). https://pubmed.ncbi.nlm.nih.gov/24953906/ DOI: 10.1016/j.thromres.2014.05.038
    Complete structured claim and evidence

  3. The isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range.

    cis-9,trans-11 conjugated linoleic acid / rumenic acid → Human platelet aggregation, agonist specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human platelet preparation.
    limitations
    Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Platelet activation changed in a laboratory assay.
    primary_references
    Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 270–276

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human platelet preparation. · source_derived_draft · unverified_draft

    ## cla-platelets-c9 Platelet activation changed in a laboratory assay. The isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range. Model: Human platelet preparation. Limitations: Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified. Evidence access: Primary abstract Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
    Complete structured claim and evidence

  4. The isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range.

    trans-10,cis-12 conjugated linoleic acid → Human platelet aggregation, agonist specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human platelet preparation.
    limitations
    Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Platelet activation changed in a laboratory assay.
    primary_references
    Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 278–284

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human platelet preparation. · source_derived_draft · unverified_draft

    ## cla-platelets-t10 Platelet activation changed in a laboratory assay. The isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range. Model: Human platelet preparation. Limitations: Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified. Evidence access: Primary abstract Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Capsaicin, N-oleoyldopamine and N-arachidonoyl-dopamine inhibited ADP-induced platelet aggregation in a concentration-dependent manner, while arachidonic-acid-induced aggregation was inhibited by capsaicin, dihydrocapsaicin and N-arachidonoyl-dopamine but not by N-oleoyldopamine, and collagen-induced aggregation was inhibited only by the endogenous vanilloids and not by capsaicin or dihydrocapsaicin.

    Dihydrocapsaicin → Capsaicin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/24953906.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717", "start_char": 0, "end_char": 1870, "text_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717"}
    experimental_model
    In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control
    exposure
    Capsaicin and dihydrocapsaicin against the endogenous vanilloids N-oleoyldopamine and N-arachidonoyl-dopamine, with ADP, collagen and arachidonic acid as agonists
    limitations
    The agonist-by-agonist design is what makes this useful: it separates the two plant compounds where a single-agonist study would have merged them. A TRPV1 antagonist control was included.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Human
    plain_language
    Capsaicin blocks clumping triggered two ways; dihydrocapsaicin blocks only one of them.
    primary_references
    [dhc-p24953906] Vanilloid-like agents inhibit aggregation of human platelets. (2014). https://pubmed.ncbi.nlm.nih.gov/24953906/ DOI: 10.1016/j.thromres.2014.05.038
    tissue_or_cell_type
    Platelets

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 153–164

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control · source_derived_draft · unverified_draft

    ### dhc-platelet-divergence Capsaicin, N-oleoyldopamine and N-arachidonoyl-dopamine inhibited ADP-induced platelet aggregation in a concentration-dependent manner, while arachidonic-acid-induced aggregation was inhibited by capsaicin, dihydrocapsaicin and N-arachidonoyl-dopamine but not by N-oleoyldopamine, and collagen-induced aggregation was inhibited only by the endogenous vanilloids and not by capsaicin or dihydrocapsaicin. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Capsaicin blocks clumping triggered two ways; dihydrocapsaicin blocks only one of them. organism: Human tissue_or_cell_type: Platelets experimental_model: In-vitro human platelet aggregation with agonist-specified stimulation and an LDH viability control limitations: The agonist-by-agonist design is what makes this useful: it separates the two plant compounds where a single-agonist study would have merged them. A TRPV1 antagonist control was included. exposure: Capsaicin and dihydrocapsaicin against the endogenous vanilloids N-oleoyldopamine and N-arachidonoyl-dopamine, with ADP, collagen and arachidonic acid as agonists evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24953906.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717", "start_char": 0, "end_char": 1870, "text_sha256": "8d11f6733abf59c36bf8e2b6ed6f44f759cab3fdd209ff3c84c21b20e178a717"} [dhc-p24953906] Vanilloid-like agents inhibit aggregation of human platelets. (2014). https://pubmed.ncbi.nlm.nih.gov/24953906/ DOI: 10.1016/j.thromres.2014.05.038
    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.

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