Component

Thromboxane A2

Thromboxane A2. Species, exposure and limitations are retained in each linked claim.

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 acts on it

  1. In human megakaryocytic cell lines a single 10 micromolar aspirin exposure suppressed thromboxane B2 by 90% and 85% respectively with full recovery within 48 to 72 hours, selective cyclooxygenase-1 inhibition by SC-560 reduced thromboxane B2 by more than 75% whereas cyclooxygenase-2 inhibition by NS-398 had minimal effect, and repeated exposure every 24 hours produced concentration- and time-dependent suppression reaching 89% by day 2 at 1 micromolar and 73% by day 4 at 0.1 micromolar, with delayed recovery likely reflecting de novo synthesis of cyclooxygenase-1 protein.

    Cyclooxygenase-1 (PTGS1) → Thromboxane A2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/41265381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc", "start_char": 0, "end_char": 2110, "text_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc"}
    experimental_model
    Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors
    exposure
    Single and repeated aspirin exposures from 0.1 to 10 micromolar, with SC-560 and NS-398 as isoform probes
    limitations
    A surrogate for a tissue that cannot ethically be sampled repeatedly. Cell lines rather than primary megakaryocytes, which the authors state.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Human cells
    plain_language
    The precursor cell makes its thromboxane with the first enzyme, and has to build new enzyme to recover.
    primary_references
    [asa-p41265381] Aspirin inhibition and recovery of cyclooxygenase activity and thromboxane biosynthesis in human megakaryocytes: a translational surrogate model. (2025). https://pubmed.ncbi.nlm.nih.gov/41265381/ DOI: 10.1016/j.jpet.2025.103762
    tissue_or_cell_type
    Megakaryocytic cell lines

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 429–440

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors · source_derived_draft · unverified_draft

    ### asa-megakaryocyte-cox1 In human megakaryocytic cell lines a single 10 micromolar aspirin exposure suppressed thromboxane B2 by 90% and 85% respectively with full recovery within 48 to 72 hours, selective cyclooxygenase-1 inhibition by SC-560 reduced thromboxane B2 by more than 75% whereas cyclooxygenase-2 inhibition by NS-398 had minimal effect, and repeated exposure every 24 hours produced concentration- and time-dependent suppression reaching 89% by day 2 at 1 micromolar and 73% by day 4 at 0.1 micromolar, with delayed recovery likely reflecting de novo synthesis of cyclooxygenase-1 protein. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The precursor cell makes its thromboxane with the first enzyme, and has to build new enzyme to recover. organism: Human cells tissue_or_cell_type: Megakaryocytic cell lines experimental_model: Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors limitations: A surrogate for a tissue that cannot ethically be sampled repeatedly. Cell lines rather than primary megakaryocytes, which the authors state. exposure: Single and repeated aspirin exposures from 0.1 to 10 micromolar, with SC-560 and NS-398 as isoform probes evidence_span: {"source_cache": "artifacts/aspirin-research/41265381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc", "start_char": 0, "end_char": 2110, "text_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc"} [asa-p41265381] Aspirin inhibition and recovery of cyclooxygenase activity and thromboxane biosynthesis in human megakaryocytes: a translational surrogate model. (2025). https://pubmed.ncbi.nlm.nih.gov/41265381/ DOI: 10.1016/j.jpet.2025.103762
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Curcumin inhibited platelet thromboxane A2 formation.

    Curcumin → Platelet thromboxane A2 production in vitro source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/curcumin-research/10484074.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a", "start_char": 0, "end_char": 1375, "text_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a"}
    experimental_model
    Isolated platelet aggregation and signaling assays
    exposure
    Curcumin: PAF/arachidonic-acid aggregation IC50 about 20-25 micromolar, thromboxane IC50 about 70 micromolar
    limitations
    In-vitro concentrations are not proof of clinical bleeding risk or an anticoagulant treatment effect; fluorescence-based calcium readout is assay-specific.
    nutrient_topic
    Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
    organism
    Platelets; donor species not resolved in indexed abstract
    plain_language
    One platelet-activating signal was reduced.
    primary_references
    [curcumin-p10484074] Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. (1999). https://pubmed.ncbi.nlm.nih.gov/10484074/ DOI: 10.1016/s0006-2952(99)00206-3
    tissue_or_cell_type
    Platelet activation and calcium signaling

    Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 996–1007

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated platelet aggregation and signaling assays · source_derived_draft · unverified_draft

    ### curcumin-platelet-thromboxane Curcumin inhibited platelet thromboxane A2 formation. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: One platelet-activating signal was reduced. organism: Platelets; donor species not resolved in indexed abstract tissue_or_cell_type: Platelet activation and calcium signaling experimental_model: Isolated platelet aggregation and signaling assays limitations: In-vitro concentrations are not proof of clinical bleeding risk or an anticoagulant treatment effect; fluorescence-based calcium readout is assay-specific. exposure: Curcumin: PAF/arachidonic-acid aggregation IC50 about 20-25 micromolar, thromboxane IC50 about 70 micromolar evidence_span: {"source_cache": "artifacts/curcumin-research/10484074.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a", "start_char": 0, "end_char": 1375, "text_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a"} [curcumin-p10484074] Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. (1999). https://pubmed.ncbi.nlm.nih.gov/10484074/ DOI: 10.1016/s0006-2952(99)00206-3
    Complete structured claim and evidence

  2. Single doses of 6 to 100 milligrams of aspirin produced a linear inhibition of platelet thromboxane B2 production ranging from 12 to 95% after 24 hours, and a daily dose of 0.45 milligrams per kilogram for 7 days produced cumulative and virtually complete inhibition without significantly reducing urinary excretion of prostaglandin E2, prostaglandin F2-alpha or 6-keto-prostaglandin F1-alpha in both men and women, an effect maintained unaltered through one month of therapy with no cumulative inhibition of renal prostaglandin synthesis, while furosemide-induced renal prostacyclin synthesis and renin release were unaffected.

    Aspirin / acetylsalicylic acid → Serum thromboxane B2 after whole blood clotting source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/aspirin-research/7045161.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb", "start_char": 0, "end_char": 1963, "text_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb"}
    experimental_model
    Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin
    exposure
    Single doses of 6 to 100 milligrams, and 0.45 milligrams per kilogram daily for 7 days and up to one month
    limitations
    The dose-ranging design across 46 subjects is what makes the selectivity claim testable. Urinary prostaglandin excretion is an indirect measure of renal synthesis.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Human
    plain_language
    A very small daily dose wipes out platelet thromboxane and leaves the kidney untouched.
    primary_references
    [asa-p7045161] Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects. (1982). https://pubmed.ncbi.nlm.nih.gov/7045161/ DOI: 10.1172/jci110576
    tissue_or_cell_type
    Platelets and kidney
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 364–375

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin · source_derived_draft · unverified_draft

    ### asa-cumulative-and-selective Single doses of 6 to 100 milligrams of aspirin produced a linear inhibition of platelet thromboxane B2 production ranging from 12 to 95% after 24 hours, and a daily dose of 0.45 milligrams per kilogram for 7 days produced cumulative and virtually complete inhibition without significantly reducing urinary excretion of prostaglandin E2, prostaglandin F2-alpha or 6-keto-prostaglandin F1-alpha in both men and women, an effect maintained unaltered through one month of therapy with no cumulative inhibition of renal prostaglandin synthesis, while furosemide-induced renal prostacyclin synthesis and renin release were unaffected. Condition category: biomarker_context nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: A very small daily dose wipes out platelet thromboxane and leaves the kidney untouched. organism: Human tissue_or_cell_type: Platelets and kidney experimental_model: Radioimmunoassay of serum thromboxane B2 and urinary prostaglandin excretion in 46 healthy subjects given single or repeated oral aspirin limitations: The dose-ranging design across 46 subjects is what makes the selectivity claim testable. Urinary prostaglandin excretion is an indirect measure of renal synthesis. exposure: Single doses of 6 to 100 milligrams, and 0.45 milligrams per kilogram daily for 7 days and up to one month evidence_span: {"source_cache": "artifacts/aspirin-research/7045161.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb", "start_char": 0, "end_char": 1963, "text_sha256": "58bb82650f675f1ba3dd21b6dcf3d83b71a56c437a687f72d2af9dcdc07abadb"} [asa-p7045161] Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects. (1982). https://pubmed.ncbi.nlm.nih.gov/7045161/ DOI: 10.1172/jci110576
    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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