Component

Prostaglandin D2

Prostaglandin D2. The model and exposure of each linked claim define its scope.

6 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 it acts on

  1. Nicotinic-acid flushing was absent in cyclooxygenase-1-deficient mice and reduced in mice lacking the tested PGD2 or PGE2 receptors, supporting prostaglandin involvement.

    Prostaglandin D2 → Nicotinic-acid-induced cutaneous flushing source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Prostaglandin E2 (additional_signal); Nicotinic acid (trigger)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"}
    experimental_model
    PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation
    exposure
    Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue
    limitations
    Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Mus musculus
    plain_language
    Nicotinic acid triggers prostaglandin signals that widen skin vessels in this mouse model.
    primary_references
    [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    tissue_or_cell_type
    Skin vasculature and hematopoietic cells

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1347–1359

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation · source_derived_draft · unverified_draft

    ### nia-clin-prostaglandin-flush Nicotinic-acid flushing was absent in cyclooxygenase-1-deficient mice and reduced in mice lacking the tested PGD2 or PGE2 receptors, supporting prostaglandin involvement. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinic acid triggers prostaglandin signals that widen skin vessels in this mouse model. organism: Mus musculus tissue_or_cell_type: Skin vasculature and hematopoietic cells experimental_model: PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation limitations: Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured. exposure: Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue cross_nutrient: Prostaglandin E2 (additional_signal); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"} [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.

    Laropiprant / MK-0524 → Cutaneous perfusion source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"}
    experimental_model
    Mouse receptor pharmacology with separate healthy-human flushing study
    exposure
    Nicotinic acid with or without the DP1 antagonist MK-0524
    limitations
    Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.
    primary_references
    [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
    tissue_or_cell_type
    Skin perfusion

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1361–1373

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse receptor pharmacology with separate healthy-human flushing study · source_derived_draft · unverified_draft

    ### nia-clin-dp1-human-flush In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes. organism: Homo sapiens tissue_or_cell_type: Skin perfusion experimental_model: Mouse receptor pharmacology with separate healthy-human flushing study limitations: Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component. exposure: Nicotinic acid with or without the DP1 antagonist MK-0524 cross_nutrient: Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"} [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
    Complete structured claim and evidence

  2. Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages.

    Diphenyleneiodonium / DPI → Prostaglandin D2 production in mouse RAW 264.7 macrophages source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Indicaxanthin 50-100 micromolar; DPI 1 micromolar; LPS 1 microgram/mL
    duration
    Indicaxanthin 1 h before LPS; PGD2 at 8 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure
    limitations
    DPI is not NOX-isoform-selective; pharmacological sensitivity does not establish NOX2 necessity or a nutrient deficiency.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure
    plain_language
    Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages.
    primary_references
    Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
    route
    In vitro co-incubation
    tissue
    Redox-dependent prostaglandin pathway
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 184–193

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure · source_derived_draft · unverified_draft

    ## indicaxanthin-dpi-pgd2-blockade Adding DPI prevented the indicaxanthin-associated increase in PGD2 production in LPS-stimulated mouse macrophages. Model/species: LPS-stimulated mouse RAW 264.7 macrophages with DPI exposure Tissue: Redox-dependent prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; DPI 1 micromolar; LPS 1 microgram/mL Route: In vitro co-incubation Duration: Indicaxanthin 1 h before LPS; PGD2 at 8 h Limits: DPI is not NOX-isoform-selective; pharmacological sensitivity does not establish NOX2 necessity or a nutrient deficiency. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  3. Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells.

    Indicaxanthin → Mouse hematopoietic prostaglandin D synthase / Hpgds source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL
    duration
    Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Mouse RAW 264.7 macrophages
    limitations
    High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Mouse RAW 264.7 macrophages
    plain_language
    Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells.
    primary_references
    Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
    route
    In vitro pretreatment then challenge
    tissue
    Cellular membranes and prostaglandin pathway

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 140–149

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft

    ## indicaxanthin-macrophage-hpgds Indicaxanthin pretreatment increased hematopoietic PGD synthase expression in LPS-stimulated RAW 264.7 cells. Model/species: Mouse RAW 264.7 macrophages Tissue: Cellular membranes and prostaglandin pathway Exposure: Indicaxanthin 50-100 micromolar; LPS 1 microgram/mL Route: In vitro pretreatment then challenge Duration: Indicaxanthin 1 h before LPS; signaling time courses 0.5-16 h Limits: High cell-culture exposure; expression changes are not direct enzyme binding. Pro-oxidant signaling in this setting differs from red-cell antioxidant preservation. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  4. Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages.

    Alpha-tocopherol → Prostaglandin D2 production in mouse RAW 264.7 macrophages source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 50-100 micromolar; alpha-tocopherol 100 micromolar; LPS 1 microgram/mL
    duration
    Indicaxanthin 1 h before LPS; lipid peroxides at 0.5 h, PGD2 at 8 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    LPS-stimulated mouse RAW 264.7 macrophages
    limitations
    Experimental vitamin E antagonism of this response is not evidence that vitamin E intake is harmful or that avoiding supplementation improves clinical outcomes.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    LPS-stimulated mouse RAW 264.7 macrophages
    plain_language
    Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages.
    primary_references
    Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004
    route
    In vitro co-incubation
    tissue
    Membrane lipid oxidation and PGD2 production

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 173–182

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · LPS-stimulated mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft

    ## indicaxanthin-vitamin-e-pgd2-antagonism Co-incubated alpha-tocopherol prevented the indicaxanthin-associated increase in PGD2 production in stimulated mouse macrophages. Model/species: LPS-stimulated mouse RAW 264.7 macrophages Tissue: Membrane lipid oxidation and PGD2 production Exposure: Indicaxanthin 50-100 micromolar; alpha-tocopherol 100 micromolar; LPS 1 microgram/mL Route: In vitro co-incubation Duration: Indicaxanthin 1 h before LPS; lipid peroxides at 0.5 h, PGD2 at 8 h Limits: Experimental vitamin E antagonism of this response is not evidence that vitamin E intake is harmful or that avoiding supplementation improves clinical outcomes. Primary reference: Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. (2014). https://pubmed.ncbi.nlm.nih.gov/25180166/ DOI: 10.1016/j.redox.2014.07.004 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  5. After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects.

    Aspirin / acetylsalicylic acid → Peptide (cysteinyl) leukotrienes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/1309968.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2", "start_char": 0, "end_char": 1685, "text_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2"}
    experimental_model
    Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects
    exposure
    12 milligrams of acetylsalicylic acid instilled nasally against saline
    limitations
    Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group.
    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
    The drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow.
    primary_references
    [asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65
    tissue_or_cell_type
    Nasal mucosa

    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 572–583

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects · source_derived_draft · unverified_draft

    ### asa-only-sensitive-patients-release After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects. 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 drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow. organism: Human tissue_or_cell_type: Nasal mucosa experimental_model: Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects limitations: Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group. exposure: 12 milligrams of acetylsalicylic acid instilled nasally against saline evidence_span: {"source_cache": "artifacts/aspirin-research/1309968.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2", "start_char": 0, "end_char": 1685, "text_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2"} [asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65
    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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