Component
Survival of a multizone perforator flap
Survival of a multizone perforator flap. 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)
Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"}
- experimental_model
- Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation
- exposure
- Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation
- limitations
- The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence.
- nutrient_topic
- Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
- organism
- Rat
- plain_language
- It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes.
- primary_references
- [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
- tissue_or_cell_type
- Skin flap vasculature
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation · source_derived_draft · unverified_draft
### dhc-suppresses-sting Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin. 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: It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes. organism: Rat tissue_or_cell_type: Skin flap vasculature experimental_model: Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation limitations: The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence. exposure: Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"} [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
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.