Component
The N-acyl ethanolamide and PPAR alpha anti-inflammatory system
The N-acyl ethanolamide and PPAR alpha anti-inflammatory system. 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.
What acts on it
Acetaminophen produced a biphasic response in the N-acyl ethanolamide and PPAR alpha system, with decreased PPAR alpha expression after 6 hours followed by a generalised increase of system components including PPAR alpha, NAPE-PLD and fatty acid amide hydrolase and of the N-acyl ethanolamides after 24 hours, confirmed in mice where gene expression of PPAR alpha and fatty acid amide hydrolase fell at 6 hours and rose by 24 hours, repeated administration decreased both and increased liver N-acyl ethanolamides with complete restoration after 15 days of rest, immunohistochemistry in a human case of acetaminophen hepatotoxicity confirmed the decrements, and damage-related alterations after repeated administration were aggravated in PPAR alpha-deficient mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/paracetamol-research/29056914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2ca7517052bab3c774f315af85f3aa8cdf810e43dc44444724bff46e2f1bdab3", "start_char": 0, "end_char": 2081, "text_sha256": "2ca7517052bab3c774f315af85f3aa8cdf810e43dc44444724bff46e2f1bdab3"}
- experimental_model
- Human HepG2 cells and mice given acute and repeated doses, with PPAR-alpha-deficient animals and a human case
- exposure
- 0.5 to 20 millimolar in cells and 750 milligrams per kilogram in mice, acute and repeated over four days
- limitations
- Follows a lipid signalling system across cells, mice, knockouts and one human case. The biphasic time course is the informative part and complicates any single-timepoint reading.
- nutrient_topic
- Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol
- organism
- Human cells, mouse and human
- plain_language
- The same lipid system that makes the painkilling metabolite is knocked down by an overdose and then rebounds, and animals lacking it fare worse.
- primary_references
- [apap-p29056914] Acetaminophen-Induced Liver Injury Alters the Acyl Ethanolamine-Based Anti-Inflammatory Signaling System in Liver. (2017). https://pubmed.ncbi.nlm.nih.gov/29056914/ DOI: 10.3389/fphar.2017.00705
- tissue_or_cell_type
- Liver
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human HepG2 cells and mice given acute and repeated doses, with PPAR-alpha-deficient animals and a human case · source_derived_draft · unverified_draft
### apap-the-lipid-brake-fails-then-rebounds Acetaminophen produced a biphasic response in the N-acyl ethanolamide and PPAR alpha system, with decreased PPAR alpha expression after 6 hours followed by a generalised increase of system components including PPAR alpha, NAPE-PLD and fatty acid amide hydrolase and of the N-acyl ethanolamides after 24 hours, confirmed in mice where gene expression of PPAR alpha and fatty acid amide hydrolase fell at 6 hours and rose by 24 hours, repeated administration decreased both and increased liver N-acyl ethanolamides with complete restoration after 15 days of rest, immunohistochemistry in a human case of acetaminophen hepatotoxicity confirmed the decrements, and damage-related alterations after repeated administration were aggravated in PPAR alpha-deficient mice. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: The same lipid system that makes the painkilling metabolite is knocked down by an overdose and then rebounds, and animals lacking it fare worse. organism: Human cells, mouse and human tissue_or_cell_type: Liver experimental_model: Human HepG2 cells and mice given acute and repeated doses, with PPAR-alpha-deficient animals and a human case limitations: Follows a lipid signalling system across cells, mice, knockouts and one human case. The biphasic time course is the informative part and complicates any single-timepoint reading. exposure: 0.5 to 20 millimolar in cells and 750 milligrams per kilogram in mice, acute and repeated over four days evidence_span: {"source_cache": "artifacts/paracetamol-research/29056914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2ca7517052bab3c774f315af85f3aa8cdf810e43dc44444724bff46e2f1bdab3", "start_char": 0, "end_char": 2081, "text_sha256": "2ca7517052bab3c774f315af85f3aa8cdf810e43dc44444724bff46e2f1bdab3"} [apap-p29056914] Acetaminophen-Induced Liver Injury Alters the Acyl Ethanolamine-Based Anti-Inflammatory Signaling System in Liver. (2017). https://pubmed.ncbi.nlm.nih.gov/29056914/ DOI: 10.3389/fphar.2017.00705
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.