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Free Radic Biol Med. 2010 Feb 15;48(4):499-505. doi: 10.1016/j.freeradbiomed.2009.11.014. Epub 2009 Nov 20.

Nitrated oleic acid up-regulates PPARgamma and attenuates experimental inflammatory bowel disease.

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  • 1Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden.

Abstract

Nitric oxide and its metabolites undergo nitration reactions with unsaturated fatty acids during oxidative inflammatory conditions, forming electrophilic nitro-fatty acid derivatives. These endogenous electrophilic mediators activate anti-inflammatory signaling reactions, serving as high-affinity ligands for peroxisome proliferator-activated receptor gamma (PPARgamma). Here we examined the therapeutic effects of 9- or 10-nitro-octadecenoic oleic acid (OA-NO(2)) and native oleic acid (OA) in a mouse model of colitis. OA-NO(2) reduced the disease activity index and completely prevented dextran sulfate sodium-induced colon shortening and the increase in colonic p65 expression. Increased PPARgamma expression was observed in colon samples as well as in cells after OA-NO(2) administration, whereas no effect was seen with OA. This induction of PPARgamma expression was completely abolished by the PPARgamma antagonist GW9662. 5-Aminosalicylic acid, an anti-inflammatory drug routinely used in the management of inflammatory bowel disease, also increased PPARgamma expression but to a lesser extent. Altogether, these findings demonstrate that administration of OA-NO(2) attenuates colonic inflammation and improves clinical symptoms in experimental inflammatory bowel disease. This protection involves activation of colonic PPARgamma.

Copyright 2009 Elsevier Inc. All rights reserved.

PMID:
19932165
[PubMed - indexed for MEDLINE]
PMCID:
PMC3290869
Free PMC Article

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