N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARα
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Laboratory animals given the TLR3 agonist poly I:C (species and numbers not stated in the abstract)
- Dose used in the study
- Oleoylethanolamide, palmitoylethanolamide or meth-anandamide given intracerebrally or systemically; doses not stated
- Duration
- Not stated in the abstract
- What was measured
- Body temperature and expression of inflammatory genes in the hypothalamus and spleen after poly I:C, with and without PPAR-alpha antagonist or agonist.
What the authors reported
This laboratory study found:
- Meth-anandamide had no effect.
- Both oleoylethanolamide and palmitoylethanolamide reduced the poly I:C fever, but only oleoylethanolamide reduced expression of fever-related genes and IRF- and NF-kappa-B-related genes in the hypothalamus; PEA did not alter these gene changes.
- Blocking PPAR-alpha prevented the oleoylethanolamide gene effects.
- The authors concluded that oleoylethanolamide, not PEA, is the main FAAH substrate modulating TLR3 neuroinflammation.
Limits of this study
An animal-model study; it cannot show effect in people. Species, numbers and doses are not stated in the abstract. PEA reduced fever but not the inflammatory gene changes. The authors declare no conflicts.
Source
PubMed 34265624 · doi:10.1016/j.jneuroim.2021.577654
Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.