Giovanna La Rana

TL;DR: It is shown that anandamide attenuates the pain behaviour produced by chemical damage to cutaneous tissue by interacting with CB1-like cannabinoid receptors located outside the CNS, and that locally generated an andamide and PEA may mediate this effect.

TL;DR: Findings indicate that PPAR-α mediates the anti-inflammatory effects of PEA and suggest that this fatty-acid ethanolamide may serve, like its analog OEA, as an endogenous ligand of PPar-α.

TL;DR: It is reported that agonists of the nuclear receptor PPAR-α (peroxisome proliferator-activated receptor-α) suppress pain behaviors induced in mice by chemical tissue injury, nerve damage, or inflammation and may represent a novel class of analgesics.

TL;DR: The endogenous fatty acid ethanolamide, palmitylethanolamide, alleviated, in a dose-dependent manner, pain behaviors elicited in mice by injections of formalin, acetic acid, kaolin, magnesium sulfate, capsaicin, and thermal nociception, and this results support the hypothesis that endogenous Palmityle Thanolamide participates in the intrinsic control of pain initiation.

TL;DR: The ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-alpha), is identified as the receptor mediating the anti-inflammatory actions of this lipid amide.