Component

Mouse inducible nitric oxide synthase / Nos2

Mouse inducible nitric oxide synthase / Nos2

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. Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study.

    Mouse peroxisome proliferator-activated receptor gamma / Pparg → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse epithelial signaling and luminal metabolite experiments.
    limitations
    Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Changing host signaling supplied a different bacterial respiratory fuel.
    primary_references
    Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 222–228

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse epithelial signaling and luminal metabolite experiments. · source_derived_draft · unverified_draft

    ## butyrate-pparg-nos2 Changing host signaling supplied a different bacterial respiratory fuel. Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study. Model: Mouse epithelial signaling and luminal metabolite experiments. Limitations: Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    Complete structured claim and evidence

  2. Numerous iNOS-positive macrophage-like cells appeared in mouse thalamus from day 10; this iNOS staining was not detected in rats.

    Thiamine (vitamin B1) → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Results: NOS Induction; Figure 3
    evidence_span
    but not in rats
    experimental_model
    Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry.
    exposure
    Dietary thiamine removal plus daily pyrithiamine in mice or rats
    limitations
    The authors could not reliably distinguish infiltrating macrophages from microglia; do not label all these cells as resident microglia.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Mus musculus
    plain_language
    An inflammatory nitric oxide synthase signal was species-specific in this study.
    primary_references
    [calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7
    tissue_or_cell_type
    Thalamic macrophage-like cells
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1211–1223

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. · source_derived_draft · unverified_draft

    ### thiamine-def-mouse-macrophagelike-nos2 Numerous iNOS-positive macrophage-like cells appeared in mouse thalamus from day 10; this iNOS staining was not detected in rats. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory nitric oxide synthase signal was species-specific in this study. organism: Mus musculus tissue_or_cell_type: Thalamic macrophage-like cells experimental_model: Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. limitations: The authors could not reliably distinguish infiltrating macrophages from microglia; do not label all these cells as resident microglia. evidence_location: Results: NOS Induction; Figure 3 evidence_span: but not in rats exposure: Dietary thiamine removal plus daily pyrithiamine in mice or rats [calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7
    Complete structured claim and evidence

  3. Nasunin reduced induced NOS2 expression.

    Nasunin → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"}
    experimental_model
    LPS-stimulated macrophage experiments
    exposure
    Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract
    limitations
    These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse RAW264 macrophages
    plain_language
    Less of the inducible nitric-oxide enzyme was measured.
    primary_references
    [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    tissue_or_cell_type
    Inflammatory mediator secretion and signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 224–235

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-stimulated macrophage experiments · source_derived_draft · unverified_draft

    ### nasunin-nos2-expression Nasunin reduced induced NOS2 expression. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less of the inducible nitric-oxide enzyme was measured. organism: Mouse RAW264 macrophages tissue_or_cell_type: Inflammatory mediator secretion and signaling experimental_model: LPS-stimulated macrophage experiments limitations: These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent. exposure: Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"} [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973
    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