Component
Adhesion of monocytes to endothelial cells
Adhesion of monocytes to endothelial cells. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
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.
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
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.