Component

Human vascular cell adhesion molecule 1 / VCAM1

Human vascular cell adhesion molecule 1 / VCAM1. Species, exposure and limitations are retained in each linked claim.

4 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. The bark oil reduced VCAM1 production in the stimulated human dermal-fibroblast system.

    Commercial C. zeylanicum bark oil in the 2017 fibroblast study → Human vascular cell adhesion molecule 1 / VCAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/28444928.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53", "start_char": 0, "end_char": 1601, "text_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53"}
    experimental_model
    Stimulated primary human dermal-fibroblast biomarker screen
    exposure
    Commercial C. zeylanicum bark oil in cell culture
    limitations
    Antiproliferative activity accompanies biomarker changes; reduced signal is not demonstrated safe wound healing or benefit from ingestion/topical use.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human
    plain_language
    This was a change in a cultured-cell inflammation model, not a demonstrated clinical skin benefit.
    primary_references
    [ceylon-p28444928] Antiinflammatory Activity of Cinnamon (Cinnamomum zeylanicum) Bark Essential Oil in a Human Skin Disease Model. (2017). https://pubmed.ncbi.nlm.nih.gov/28444928/ DOI: 10.1002/ptr.5822
    tissue_or_cell_type
    Dermal fibroblast inflammatory/fibrotic model

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 1013–1024

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stimulated primary human dermal-fibroblast biomarker screen · source_derived_draft · unverified_draft

    ### ceylon-vcam1 The bark oil reduced VCAM1 production in the stimulated human dermal-fibroblast system. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: This was a change in a cultured-cell inflammation model, not a demonstrated clinical skin benefit. organism: Human tissue_or_cell_type: Dermal fibroblast inflammatory/fibrotic model experimental_model: Stimulated primary human dermal-fibroblast biomarker screen limitations: Antiproliferative activity accompanies biomarker changes; reduced signal is not demonstrated safe wound healing or benefit from ingestion/topical use. exposure: Commercial C. zeylanicum bark oil in cell culture evidence_span: {"source_cache": "artifacts/ceylon-research/28444928.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53", "start_char": 0, "end_char": 1601, "text_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53"} [ceylon-p28444928] Antiinflammatory Activity of Cinnamon (Cinnamomum zeylanicum) Bark Essential Oil in a Human Skin Disease Model. (2017). https://pubmed.ncbi.nlm.nih.gov/28444928/ DOI: 10.1002/ptr.5822
    Complete structured claim and evidence

  2. Ergothioneine at 0.1-0.3 mM reduced IL-1beta-induced vascular cell adhesion molecule 1 expression in human aortic endothelial cells.

    L-Ergothioneine → Human vascular cell adhesion molecule 1 / VCAM1 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 320–326

    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-human-vcam1 The endothelial surface expressed fewer adhesion signals. Ergothioneine at 0.1-0.3 mM reduced IL-1beta-induced vascular cell adhesion molecule 1 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

  3. Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs.

    Indicaxanthin → Human vascular cell adhesion molecule 1 / VCAM1 source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
    duration
    1 h pretreatment followed by 16 h oxidized-LDL exposure
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human umbilical vein endothelial cells / HUVECs
    limitations
    Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human umbilical vein endothelial cells / HUVECs
    plain_language
    Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs.
    primary_references
    Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
    route
    In vitro pretreatment and challenge
    tissue
    Endothelial culture

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 371–380

    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 · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft

    ## indicaxanthin-endothelial-vcam1 Indicaxanthin pretreatment reduced oxidized-LDL-induced VCAM1 mRNA and protein increases in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Tumour necrosis factor alpha induced Ser536 phosphorylation of p65 NF-kappa-B, expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1, and interleukin 6 production in primary human endothelial cells, and these effects were robustly abrogated by dihydrocapsaicin, which also led to a marked reduction in tumour-necrosis-factor-mediated monocyte adhesion to endothelial cells.

    Dihydrocapsaicin → Endothelial activation by tumour necrosis factor alpha source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"}
    experimental_model
    Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays
    exposure
    Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C
    limitations
    The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Human
    plain_language
    Below the toxic range it calms the inflamed vessel lining and stops immune cells sticking to it.
    primary_references
    [dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521
    tissue_or_cell_type
    Vascular endothelium

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 673–684

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays · source_derived_draft · unverified_draft

    ### dhc-endothelial-anti-inflammatory Tumour necrosis factor alpha induced Ser536 phosphorylation of p65 NF-kappa-B, expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1, and interleukin 6 production in primary human endothelial cells, and these effects were robustly abrogated by dihydrocapsaicin, which also led to a marked reduction in tumour-necrosis-factor-mediated monocyte adhesion to endothelial cells. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Below the toxic range it calms the inflamed vessel lining and stops immune cells sticking to it. organism: Human tissue_or_cell_type: Vascular endothelium experimental_model: Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays limitations: The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here. exposure: Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"} [dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521
    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