Thromboxane B2

duration

Not stated here

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

experimental_model

Rabbit washed platelets

exposure

Nattokinase

limitations

The authors read this as blockade of thromboxane formation upstream of aggregation, but the enzyme or pathway step that is blocked is not shown. Concentrations used in vitro are high relative to anything measured in plasma after oral dosing.

organism

Rabbit washed platelets

plain_language

Nattokinase reduced thromboxane B2 formation from collagen-activated platelets in a concentration-dependent manner.

primary_references

Nattokinase improves blood flow by inhibiting platelet aggregation and thrombus formation. (2013) https://pubmed.ncbi.nlm.nih.gov/24396387/ DOI: 10.5625/lar.2013.29.4.221

route

In vitro

tissue

Thromboxane B2 assay

Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 345–345

Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Rabbit washed platelets · source_derived_draft · unverified_draft

Nattokinase reduced thromboxane B2 formation from collagen-activated platelets in a concentration-dependent manner.

cross_nutrient

false

experimental_model

Washed rat platelet stimulation and TXB2 enzyme immunoassay

exposure

25 min compound preincubation at 37°C; 1–2 µM A23187 with 1–2 mM CaCl2 for 10 min.

limitations

TXB2 is a stable surrogate for TXA2 production; neither clinical bleeding nor platelet aggregation was measured in this endpoint. Isolated rat platelets do not establish human antithrombotic benefit.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Rattus norvegicus

plain_language

The metabolite reduced a measured marker of thromboxane production in isolated rat platelets.

primary_references

[park2022] Different forms of vitamin E and metabolite 13'-carboxychromanols inhibit cyclooxygenase-1 and its catalyzed thromboxane in platelets, and tocotrienols and 13'-carboxychromanols are competitive inhibitors of 5-lipoxygenase. (2022). https://pubmed.ncbi.nlm.nih.gov/34710615/ DOI: 10.1016/j.jnutbio.2021.108884

tissue_or_cell_type

Isolated blood platelets

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1076–1087

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Washed rat platelet stimulation and TXB2 enzyme immunoassay · source_derived_draft · unverified_draft

### e-sig-delta-acid-platelet-txb2 Delta-tocopherol-13′-carboxychromanol reduced A23187-stimulated TXB2 output from washed rat platelets, with the metabolite experiments reporting IC50 values in the 1.5–2.5 µM range. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The metabolite reduced a measured marker of thromboxane production in isolated rat platelets. organism: Rattus norvegicus tissue_or_cell_type: Isolated blood platelets experimental_model: Washed rat platelet stimulation and TXB2 enzyme immunoassay limitations: TXB2 is a stable surrogate for TXA2 production; neither clinical bleeding nor platelet aggregation was measured in this endpoint. Isolated rat platelets do not establish human antithrombotic benefit. exposure: 25 min compound preincubation at 37°C; 1–2 µM A23187 with 1–2 mM CaCl2 for 10 min. cross_nutrient: false [park2022] Different forms of vitamin E and metabolite 13'-carboxychromanols inhibit cyclooxygenase-1 and its catalyzed thromboxane in platelets, and tocotrienols and 13'-carboxychromanols are competitive inhibitors of 5-lipoxygenase. (2022). https://pubmed.ncbi.nlm.nih.gov/34710615/ DOI: 10.1016/j.jnutbio.2021.108884

evidence_span

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experimental_model

Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices

exposure

800 milligrams ibuprofen against 100, 400 or 800 milligrams celecoxib

limitations

Measures both isoform-specific indices in the same people, which is what allows the prostacyclin source to be assigned. Acute dosing in healthy volunteers.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

The enzyme these drugs are meant to spare the stomach by blocking is the one that makes the body’s main anticlotting prostaglandin.

primary_references

[ibu-p9874808] Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2. (1999). https://pubmed.ncbi.nlm.nih.gov/9874808/ DOI: 10.1073/pnas.96.1.272

tissue_or_cell_type

Platelets and whole body

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 526–537

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices · source_derived_draft · unverified_draft

### ibu-cox2-makes-the-prostacyclin Ibuprofen but not celecoxib significantly inhibited thromboxane-dependent platelet aggregation induced ex vivo by arachidonic acid, 83% against 11.9%, and reduced serum thromboxane B2 by 95% and urinary 11-dehydro thromboxane B2 by 70%, while both ibuprofen and celecoxib suppressed an index of cyclooxygenase-2 activity to a comparable degree and both suppressed urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha, data suggesting that cyclooxygenase-2 is a major source of systemic prostacyclin biosynthesis in healthy humans. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The enzyme these drugs are meant to spare the stomach by blocking is the one that makes the body’s main anticlotting prostaglandin. organism: Human tissue_or_cell_type: Platelets and whole body experimental_model: Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices limitations: Measures both isoform-specific indices in the same people, which is what allows the prostacyclin source to be assigned. Acute dosing in healthy volunteers. exposure: 800 milligrams ibuprofen against 100, 400 or 800 milligrams celecoxib evidence_span: {"source_cache": "artifacts/ibuprofen-research/9874808.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4", "start_char": 0, "end_char": 1789, "text_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4"} [ibu-p9874808] Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2. (1999). https://pubmed.ncbi.nlm.nih.gov/9874808/ DOI: 10.1073/pnas.96.1.272

evidence_span

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experimental_model

Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma

exposure

Indomethacin and ibuprofen compared, with isolated platelets and platelet microsomes

limitations

The resuspension experiment is what separates a reversible inhibitor from a slowly reversible one. It uses indomethacin as the contrast and reports ibuprofen as the reference reversible drug.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

Wash the drug away and the platelet enzyme is working again at once, which is the opposite of what aspirin does.

primary_references

[ibu-p3088675] Time-dependent inhibition of platelet cyclooxygenase by indomethacin is slowly reversible. (1986). https://pubmed.ncbi.nlm.nih.gov/3088675/ DOI: 10.1016/0090-6980(86)90170-x

tissue_or_cell_type

Platelets

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 279–290

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma · source_derived_draft · unverified_draft

### ibu-ibuprofen-washes-straight-out When platelets were isolated and resuspended in homologous drug-free plasma, slow recovery of thromboxane production was seen after indomethacin with 50% of control activity regained in 100 minutes, whereas ibuprofen-treated platelets, exposed to a competitive inhibitor of cyclooxygenase, recovered nearly completely immediately on being resuspended in drug-free plasma. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: Wash the drug away and the platelet enzyme is working again at once, which is the opposite of what aspirin does. organism: Human tissue_or_cell_type: Platelets experimental_model: Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma limitations: The resuspension experiment is what separates a reversible inhibitor from a slowly reversible one. It uses indomethacin as the contrast and reports ibuprofen as the reference reversible drug. exposure: Indomethacin and ibuprofen compared, with isolated platelets and platelet microsomes evidence_span: {"source_cache": "artifacts/ibuprofen-research/3088675.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a", "start_char": 0, "end_char": 1400, "text_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a"} [ibu-p3088675] Time-dependent inhibition of platelet cyclooxygenase by indomethacin is slowly reversible. (1986). https://pubmed.ncbi.nlm.nih.gov/3088675/ DOI: 10.1016/0090-6980(86)90170-x

evidence_span

{"source_cache": "artifacts/ibuprofen-research/8907587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75", "start_char": 0, "end_char": 1101, "text_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75"}

experimental_model

Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices

exposure

Lipopolysaccharide induction of cyclooxygenase-2 with a single oral indomethacin dose ex vivo

limitations

Establishes the assay the other records rely on. Indomethacin rather than ibuprofen is the drug dosed here.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

The first enzyme is always there and the second one appears when tissue is provoked; most of these drugs hit the first harder.

primary_references

[ibu-p8907587] A human whole blood assay for clinical evaluation of biochemical efficacy of cyclooxygenase inhibitors. (1996). https://pubmed.ncbi.nlm.nih.gov/8907587/ DOI: 10.1007/bf02265118

tissue_or_cell_type

Whole blood and mononuclear cells

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 357–368

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices · source_derived_draft · unverified_draft

### ibu-most-nsaids-favour-cox1 Incubation of human mononuclear cells with lipopolysaccharide induced a time-dependent increase in cyclooxygenase-2 protein of more than a hundredfold at 24 hours with increased prostaglandin E2 production, while cyclooxygenase-1 protein was present at time zero and not induced, and most non-steroidal anti-inflammatory drugs are more potent at inhibiting cyclooxygenase-1 than cyclooxygenase-2, with five experimental compounds showing greater selectivity for cyclooxygenase-2. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The first enzyme is always there and the second one appears when tissue is provoked; most of these drugs hit the first harder. organism: Human tissue_or_cell_type: Whole blood and mononuclear cells experimental_model: Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices limitations: Establishes the assay the other records rely on. Indomethacin rather than ibuprofen is the drug dosed here. exposure: Lipopolysaccharide induction of cyclooxygenase-2 with a single oral indomethacin dose ex vivo evidence_span: {"source_cache": "artifacts/ibuprofen-research/8907587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75", "start_char": 0, "end_char": 1101, "text_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75"} [ibu-p8907587] A human whole blood assay for clinical evaluation of biochemical efficacy of cyclooxygenase inhibitors. (1996). https://pubmed.ncbi.nlm.nih.gov/8907587/ DOI: 10.1007/bf02265118

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/12152005.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da", "start_char": 0, "end_char": 1822, "text_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da"}

experimental_model

Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants

exposure

600 milligrams oral racemic ibuprofen, with thromboxane B2 and prostaglandin E2 measured ex vivo

limitations

Links a genotype to both the drug level and the enzyme effect in the same subjects. Twenty-one volunteers spread across genotype groups, so each group is small.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

People who clear the active half slowly get both more drug and more effect from the same tablet.

primary_references

[ibu-p12152005] Enantiospecific effects of cytochrome P450 2C9 amino acid variants on ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2. (2002). https://pubmed.ncbi.nlm.nih.gov/12152005/ DOI: 10.1067/mcp.2002.125726

tissue_or_cell_type

Plasma, platelets and monocytes

trigger_kind

machinery_impairment Imported condition classification; unverified.

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 214–225

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants · source_derived_draft · unverified_draft

### ibu-slow-clearance-more-effect Population mean S-ibuprofen clearances were 3.25, 2.38 and 1.52 litres per hour in carriers of CYP2C9 genotypes *1/*1, *1/*3 and *3/*3 respectively while the *2 variant had no significant effect, and ex vivo formation of thromboxane B2 reflecting cyclooxygenase-1 inhibition depended significantly on the polymorphism, with maximal inhibition and the area under the effect-time curve larger in carriers of the slow genotypes, the same trend holding for prostaglandin E2. Condition category: machinery_impairment nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: People who clear the active half slowly get both more drug and more effect from the same tablet. organism: Human tissue_or_cell_type: Plasma, platelets and monocytes experimental_model: Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants limitations: Links a genotype to both the drug level and the enzyme effect in the same subjects. Twenty-one volunteers spread across genotype groups, so each group is small. exposure: 600 milligrams oral racemic ibuprofen, with thromboxane B2 and prostaglandin E2 measured ex vivo evidence_span: {"source_cache": "artifacts/ibuprofen-research/12152005.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da", "start_char": 0, "end_char": 1822, "text_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da"} [ibu-p12152005] Enantiospecific effects of cytochrome P450 2C9 amino acid variants on ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2. (2002). https://pubmed.ncbi.nlm.nih.gov/12152005/ DOI: 10.1067/mcp.2002.125726

evidence_span

{"source_cache": "artifacts/paracetamol-research/12598417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5796a25a03c77d12e8376a60aa094e481bd0c2ab58b29ddcb70027ab477b267", "start_char": 0, "end_char": 1894, "text_sha256": "e5796a25a03c77d12e8376a60aa094e481bd0c2ab58b29ddcb70027ab477b267"}

experimental_model

Human whole blood and isolated monocytes and platelets with parallel prostaglandin E2 and thromboxane B2 measurement

exposure

Acetaminophen at therapeutic plasma concentrations of 100 and 300 micromolar, in whole blood and in isolated cells

limitations

The whole blood against isolated cell comparison shows plasma components matter, and measuring two prostanoids in parallel separates the synthase from the downstream synthase. Ex vivo only.

nutrient_topic

Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol

organism

Human

plain_language

In whole blood it nearly abolishes the inflammatory prostaglandin; in isolated cells it manages only sixty per cent.

primary_references

[apap-p12598417] Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells. (2003). https://pubmed.ncbi.nlm.nih.gov/12598417/ DOI: 10.1038/sj.bjp.0705078

tissue_or_cell_type

Monocytes and platelets

Paracetamol: the enzyme it reduces rather than blocks, the isoform that turned out not to exist, the metabolite that carries the analgesia, and the metabolite that destroys the liver (2026-09-22) · lines 272–283

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human whole blood and isolated monocytes and platelets with parallel prostaglandin E2 and thromboxane B2 measurement · source_derived_draft · unverified_draft

### apap-plasma-changes-the-answer Acetaminophen inhibited lipopolysaccharide-induced whole blood prostaglandin E2 and thromboxane B2 production with half-maximal inhibitory concentrations of 44 and 94 micromolar, at therapeutic concentrations of 100 and 300 micromolar it reduced prostaglandin E2 more than thromboxane B2, but in isolated monocytes both were maximally reduced by only 60%, and at the same concentrations it caused a similar and incomplete inhibition of platelet prostaglandin E2 and thromboxane B2 during whole blood clotting, so that in the presence of plasma the drug almost completely suppressed inducible prostaglandin E2 biosynthesis through effects on both cyclooxygenase-2 and inducible prostaglandin E synthase. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: In whole blood it nearly abolishes the inflammatory prostaglandin; in isolated cells it manages only sixty per cent. organism: Human tissue_or_cell_type: Monocytes and platelets experimental_model: Human whole blood and isolated monocytes and platelets with parallel prostaglandin E2 and thromboxane B2 measurement limitations: The whole blood against isolated cell comparison shows plasma components matter, and measuring two prostanoids in parallel separates the synthase from the downstream synthase. Ex vivo only. exposure: Acetaminophen at therapeutic plasma concentrations of 100 and 300 micromolar, in whole blood and in isolated cells evidence_span: {"source_cache": "artifacts/paracetamol-research/12598417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5796a25a03c77d12e8376a60aa094e481bd0c2ab58b29ddcb70027ab477b267", "start_char": 0, "end_char": 1894, "text_sha256": "e5796a25a03c77d12e8376a60aa094e481bd0c2ab58b29ddcb70027ab477b267"} [apap-p12598417] Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells. (2003). https://pubmed.ncbi.nlm.nih.gov/12598417/ DOI: 10.1038/sj.bjp.0705078

evidence_access

Primary abstract

experimental_model

Human platelet radiotracer assay.

limitations

TXB2 is the measured readout of TXA2 formation.

nutrient_topic

CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family

plain_language

Two branches from the same fatty acid responded differently.

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 286–292

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

## cla-txb2 Two branches from the same fatty acid responded differently. The mixture and individual isomers reduced arachidonate-derived TXB2 formation, while platelet 12-HETE formation was not inhibited. Model: Human platelet radiotracer assay. Limitations: TXB2 is the measured readout of TXA2 formation. 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

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