Component
15R-prostaglandin D2
15R-prostaglandin D2. Species, exposure and limitations are retained in each linked claim.
1 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Aspirin increased 15R-prostaglandin D2 but not 15R-prostaglandin E2 in isolated human leukocytes activated with lipopolysaccharide to induce cyclooxygenase-2, and 15R-prostaglandin D2 inhibited human platelet aggregation induced by the thromboxane receptor agonist U46,619, an effect abrogated by an antagonist of the DP1 prostanoid receptor, so 15R-prostaglandins are novel products of aspirin therapy that may contribute to its antiplatelet and other effects.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/aspirin-research/30096040.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8", "start_char": 0, "end_char": 1666, "text_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8"}
- experimental_model
- Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays
- exposure
- Aspirin acetylation, with lipopolysaccharide-induced cyclooxygenase-2 in leukocytes and a thromboxane receptor agonist on platelets
- limitations
- Shows the acetylated enzyme keeps more of its original chemistry than the HETE story implies, and links the product to a measured platelet effect. Isolated cells rather than treated people.
- 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
- One of those mirror-image products is itself an antiplatelet agent, working through a different receptor.
- primary_references
- [asa-p30096040] Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. (2019). https://pubmed.ncbi.nlm.nih.gov/30096040/ DOI: 10.1096/fj.201801018r
- tissue_or_cell_type
- Recombinant enzyme and isolated leukocytes and platelets
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays · source_derived_draft · unverified_draft
### asa-15r-pgd2-blocks-platelets Aspirin increased 15R-prostaglandin D2 but not 15R-prostaglandin E2 in isolated human leukocytes activated with lipopolysaccharide to induce cyclooxygenase-2, and 15R-prostaglandin D2 inhibited human platelet aggregation induced by the thromboxane receptor agonist U46,619, an effect abrogated by an antagonist of the DP1 prostanoid receptor, so 15R-prostaglandins are novel products of aspirin therapy that may contribute to its antiplatelet and other effects. 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: One of those mirror-image products is itself an antiplatelet agent, working through a different receptor. organism: Human tissue_or_cell_type: Recombinant enzyme and isolated leukocytes and platelets experimental_model: Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays limitations: Shows the acetylated enzyme keeps more of its original chemistry than the HETE story implies, and links the product to a measured platelet effect. Isolated cells rather than treated people. exposure: Aspirin acetylation, with lipopolysaccharide-induced cyclooxygenase-2 in leukocytes and a thromboxane receptor agonist on platelets evidence_span: {"source_cache": "artifacts/aspirin-research/30096040.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8", "start_char": 0, "end_char": 1666, "text_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8"} [asa-p30096040] Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. (2019). https://pubmed.ncbi.nlm.nih.gov/30096040/ DOI: 10.1096/fj.201801018r
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.