Component

Human intercellular adhesion molecule 1 / ICAM1

Human intercellular adhesion molecule 1 / ICAM1. Species, exposure and limitations are retained in each linked claim.

7 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. Adding L-cysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    L-Cysteine → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 236–242

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-cysteine-icam-rescue A separately stored thiol changed the signaling result. Adding L-cysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  2. Adding glutathione attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    GSH → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 220–226

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-gsh-icam-rescue A separately stored thiol changed the signaling result. Adding glutathione attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  3. Cucurbitacin B decreased ICAM1 expression induced by TNF-alpha or IL-1-alpha in human A549 cells.

    Cucurbitacin B → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human lung adenocarcinoma cell model.
    limitations
    This is not a clinical anti-inflammatory outcome.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A cell-adhesion response to inflammatory signals decreased.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 212–218

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human lung adenocarcinoma cell model. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-icam A cell-adhesion response to inflammatory signals decreased. Cucurbitacin B decreased ICAM1 expression induced by TNF-alpha or IL-1-alpha in human A549 cells. Model: Human lung adenocarcinoma cell model. Limitations: This is not a clinical anti-inflammatory outcome. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  4. Adding N-acetylcysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols.

    N-Acetyl-L-cysteine → Human intercellular adhesion molecule 1 / ICAM1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human A549 cytokine-stimulation experiment.
    limitations
    The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    A separately stored thiol changed the signaling result.
    primary_references
    Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 228–234

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 cytokine-stimulation experiment. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-nac-icam-rescue A separately stored thiol changed the signaling result. Adding N-acetylcysteine attenuated cucurbitacin B inhibition of TNF-alpha-induced ICAM1 expression; L-cysteine had a smaller effect than the other tested thiols. Model: Human A549 cytokine-stimulation experiment. Limitations: The experiment supports a chemical-reactivity dependency; it does not establish a human supplement interaction magnitude. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
    Complete structured claim and evidence

  5. The bark oil reduced ICAM1 production in the stimulated human dermal-fibroblast system.

    Commercial C. zeylanicum bark oil in the 2017 fibroblast study → Human intercellular adhesion molecule 1 / ICAM1 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 1026–1037

    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-icam1 The bark oil reduced ICAM1 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

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

    L-Ergothioneine → Human intercellular adhesion molecule 1 / ICAM1 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 328–334

    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-icam1 The endothelial surface expressed fewer adhesion signals. Ergothioneine at 0.1-0.3 mM reduced IL-1beta-induced intercellular 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

  7. Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 mRNA and protein increases in HUVECs.

    Indicaxanthin → Human intercellular adhesion molecule 1 / ICAM1 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 ICAM1 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 360–369

    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-icam1 Indicaxanthin pretreatment reduced oxidized-LDL-induced ICAM1 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

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