Component
Caffeic acid phenethyl ester / CAPE
Caffeic acid phenethyl ester / CAPE
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.
What it acts on
CAPE blocked the ALCAR-associated rise in Grm2 transcript in DRG cultures.
Experimental context and source evidence
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_condition
- ALCAR without CAPE pretreatment · Caffeic acid phenethyl ester / CAPE Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_condition
- ALCAR without CAPE 250 micromolar · Acetyl-L-carnitine Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "CAPE pretreatment plus ALCAR", "comparator": "ALCAR without CAPE", "endpoint": "CAPE blocked the ALCAR-associated rise in Grm2 transcript in DRG cultures.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "caffeic-acid-phenethyl-ester", "state": "pretreatment"}, {"entity_slug": "acetylcarnitine", "state": "250 micromolar"}]} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- CAPE 2.5 micrograms/mL for 30 min before 250 micromolar ALCAR; 1-h transcript measurement.
- interpretation_status
- Source-derived curation with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
- plain_language
- CAPE blocked the ALCAR-associated rise in Grm2 transcript in DRG cultures.
- primary_references
- Transcriptional regulation of metabotropic glutamate receptor 2/3 expression by the NF-kappaB pathway in primary dorsal root ganglia neurons: a possible mechanism for the analgesic effect of L-acetylcarnitine. | https://pubmed.ncbi.nlm.nih.gov/16764720/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC1550235/ | https://doi.org/10.1186/1744-8069-2-20
- source_locator
- Reviewed reference drg-cape; Pharmacological NF-kappaB inhibition is not a selective genetic test of one acetylation site.
Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 216–222
AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · CAPE 2.5 micrograms/mL for 30 min before 250 micromolar ALCAR; 1-h transcript measurement. · Recorded from source · Recorded from source
### drg-cape CAPE blocked the ALCAR-associated rise in Grm2 transcript in DRG cultures. Pharmacological NF-kappaB inhibition is not a selective genetic test of one acetylation site. Model and exposure: CAPE 2.5 micrograms/mL for 30 min before 250 micromolar ALCAR; 1-h transcript measurement. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptional regulation of metabotropic glutamate receptor 2/3 expression by the NF-kappaB pathway in primary dorsal root ganglia neurons: a possible mechanism for the analgesic effect of L-acetylcarnitine. | 2006 | https://pubmed.ncbi.nlm.nih.gov/16764720/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC1550235/ | https://doi.org/10.1186/1744-8069-2-20 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
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.