Component

Human E-selectin

Context-specific entity; species, compartment and exposure are stated on each claim.

2 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. Ergothioneine at 0.1-0.3 mM reduced IL-1beta-induced E-selectin expression in human aortic endothelial cells.

    L-Ergothioneine → Human E-selectin source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    16-hour pretreatment, then 6-hour cytokine challenge.
    limitations
    Cell-culture result; not established prevention of human atherosclerosis.
    nutrient_topic
    Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
    plain_language
    The endothelial surface expressed fewer adhesion signals.
    primary_references
    The bioactive agent ergothioneine, a key component of dietary mushrooms, inhibits monocyte binding to endothelial cells characteristic of early cardiovascular disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21091247/ · DOI 10.1089/jmf.2009.0194

    Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 336–342

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 16-hour pretreatment, then 6-hour cytokine challenge. · source_derived_draft · unverified_draft

    ## ergothioneine-adhesion-sele The endothelial surface expressed fewer adhesion signals. Ergothioneine at 0.1-0.3 mM reduced IL-1beta-induced E-selectin expression in human aortic endothelial cells. Model: 16-hour pretreatment, then 6-hour cytokine challenge. Limitations: Cell-culture result; not established prevention of human atherosclerosis. Evidence access: Primary abstract The bioactive agent ergothioneine, a key component of dietary mushrooms, inhibits monocyte binding to endothelial cells characteristic of early cardiovascular disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21091247/ · DOI 10.1089/jmf.2009.0194
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Sodium salicylate inhibited activation of nuclear factor kappa B by preventing phosphorylation and subsequent degradation of I-kappa-B-alpha without affecting tumour necrosis factor alpha-induced phosphorylation of ATF-2, blocked the increase in adhesion molecule messenger RNA and gave dose-dependent inhibition of surface vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 with higher doses required for endothelial-leukocyte adhesion molecule 1, and inhibited transendothelial migration of neutrophils; indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression, suggesting the effects were not due to inhibition of cyclooxygenase.

    Salicylate / salicylic acid → Surface expression of endothelial leukocyte adhesion molecules source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/8621937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1", "start_char": 0, "end_char": 1767, "text_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1"}
    experimental_model
    Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells
    exposure
    Sodium salicylate against tumour necrosis factor alpha stimulation, with indomethacin as a cyclooxygenase control
    limitations
    The indomethacin control is the important part: it shows the effect is not a cyclooxygenase effect. High salicylate concentrations, which the authors relate to high-dose therapy rather than to antiplatelet dosing.
    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
    A cyclooxygenase blocker does nothing here, so this arm of salicylate is not about prostaglandins at all.
    primary_references
    [asa-p8621937] Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration. (1996). https://pubmed.ncbi.nlm.nih.gov/8621937/ DOI: 10.4049/jimmunol.156.10.3961
    tissue_or_cell_type
    Endothelium

    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 481–492

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells · source_derived_draft · unverified_draft

    ### asa-not-a-cyclooxygenase-effect Sodium salicylate inhibited activation of nuclear factor kappa B by preventing phosphorylation and subsequent degradation of I-kappa-B-alpha without affecting tumour necrosis factor alpha-induced phosphorylation of ATF-2, blocked the increase in adhesion molecule messenger RNA and gave dose-dependent inhibition of surface vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 with higher doses required for endothelial-leukocyte adhesion molecule 1, and inhibited transendothelial migration of neutrophils; indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression, suggesting the effects were not due to inhibition of cyclooxygenase. 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: A cyclooxygenase blocker does nothing here, so this arm of salicylate is not about prostaglandins at all. organism: Human cells tissue_or_cell_type: Endothelium experimental_model: Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells limitations: The indomethacin control is the important part: it shows the effect is not a cyclooxygenase effect. High salicylate concentrations, which the authors relate to high-dose therapy rather than to antiplatelet dosing. exposure: Sodium salicylate against tumour necrosis factor alpha stimulation, with indomethacin as a cyclooxygenase control evidence_span: {"source_cache": "artifacts/aspirin-research/8621937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1", "start_char": 0, "end_char": 1767, "text_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1"} [asa-p8621937] Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration. (1996). https://pubmed.ncbi.nlm.nih.gov/8621937/ DOI: 10.4049/jimmunol.156.10.3961
    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