In:
British Journal of Pharmacology, Wiley, Vol. 172, No. 1 ( 2015-01), p. 142-158
Abstract:
Palmitoylethanolamide ( PEA ) acts via several targets, including cannabinoid CB 1 and CB 2 receptors, transient receptor potential vanilloid type‐1 ( TRPV1 ) ion channels, peroxisome proliferator‐activated receptor alpha ( PPAR α ) and orphan G protein‐coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation. Here, we investigated the effect of PEA in a murine model of colitis. Experimental Approach Colitis was induced in mice by intracolonic administration of dinitrobenzenesulfonic acid ( DNBS ). Inflammation was assessed by evaluating inflammatory markers/parameters and by histology; intestinal permeability by a fluorescent method; colonic cell proliferation by immunohistochemistry; PEA and endocannabinoid levels by liquid chromatography mass spectrometry; receptor and enzyme mRNA expression by quantitative RT‐ PCR . Key Results DNBS administration caused inflammatory damage, increased colonic levels of PEA and endocannabinoids, down‐regulation of mRNA for TRPV1 and GPR55 but no changes in mRNA for CB 1 , CB 2 and PPARα . Exogenous PEA (i.p. and/or p.o., 1 mg·kg −1 ) attenuated inflammation and intestinal permeability, stimulated colonic cell proliferation, and increased colonic TRPV1 and CB 1 receptor expression. The anti‐inflammatory effect of PEA was attenuated or abolished by CB 2 receptor, GPR55 or PPARα antagonists and further increased by the TRPV1 antagonist capsazepine. Conclusions and Implications PEA improves murine experimental colitis, the effect being mediated by CB 2 receptors, GPR55 and PPARα , and modulated by TRPV1 channels.
Type of Medium:
Online Resource
ISSN:
0007-1188
,
1476-5381
DOI:
10.1111/bph.2015.172.issue-1
Language:
English
Publisher:
Wiley
Publication Date:
2015
detail.hit.zdb_id:
2029728-2
SSG:
15,3
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