Component

Megakaryocyte

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

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 it acts on

  1. Megakaryocyte thromboxane production was depressed by 70% and that of platelets by 85% at two hours after 20 milligrams per kilogram oral aspirin, full megakaryocyte thromboxane recovery occurred by 72 hours and preceded complete platelet recovery by 24 hours, megakaryocyte synthesis showed substantial recovery by 36 hours while platelet recovery did not begin for 24 hours, and the authors conclude that thromboxane synthesis develops in rat megakaryocytes after approximately 48 hours of cytoplasmic differentiation toward platelet shedding.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/6812167.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389", "start_char": 0, "end_char": 1366, "text_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389"}
    experimental_model
    Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose
    exposure
    20 milligrams per kilogram oral aspirin dissolved in dimethyl sulphoxide
    limitations
    Follows the precursor cell rather than the platelet, which is where the recovery kinetics are actually set. A rat study and the maturation timing is inferred from transit times.
    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
    Rat
    plain_language
    The marrow recovers first and the blood follows, because new platelets have to be built and released.
    primary_references
    [asa-p6812167] Aspirin inhibits rat megakaryocyte thromboxane synthesis. (1982). https://pubmed.ncbi.nlm.nih.gov/6812167/ DOI: 10.1016/0090-6980(82)90128-9
    tissue_or_cell_type
    Bone marrow megakaryocytes and platelets

    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 416–427

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose · source_derived_draft · unverified_draft

    ### asa-recovery-starts-in-the-marrow Megakaryocyte thromboxane production was depressed by 70% and that of platelets by 85% at two hours after 20 milligrams per kilogram oral aspirin, full megakaryocyte thromboxane recovery occurred by 72 hours and preceded complete platelet recovery by 24 hours, megakaryocyte synthesis showed substantial recovery by 36 hours while platelet recovery did not begin for 24 hours, and the authors conclude that thromboxane synthesis develops in rat megakaryocytes after approximately 48 hours of cytoplasmic differentiation toward platelet shedding. 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 marrow recovers first and the blood follows, because new platelets have to be built and released. organism: Rat tissue_or_cell_type: Bone marrow megakaryocytes and platelets experimental_model: Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose limitations: Follows the precursor cell rather than the platelet, which is where the recovery kinetics are actually set. A rat study and the maturation timing is inferred from transit times. exposure: 20 milligrams per kilogram oral aspirin dissolved in dimethyl sulphoxide evidence_span: {"source_cache": "artifacts/aspirin-research/6812167.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389", "start_char": 0, "end_char": 1366, "text_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389"} [asa-p6812167] Aspirin inhibits rat megakaryocyte thromboxane synthesis. (1982). https://pubmed.ncbi.nlm.nih.gov/6812167/ DOI: 10.1016/0090-6980(82)90128-9
    Complete structured claim and evidence

Where it participates (unsigned role)

  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

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