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Mediators of Inflammation
Volume 2013, Article ID 513251, 10 pages
http://dx.doi.org/10.1155/2013/513251
Research Article

Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome

1Department of Pathology, School of Medicine, National University of Cuyo, Avenida Libertador No. 80, Centro Universitario, CP 5500 Mendoza, Argentina
2Institute of Experimental Medicine and Biology of Cuyo (IMBECU)-CONICET, Mendoza, Argentina
3Department of Morphophysiology, School of Medicine, National University of Cuyo, Avenida Libertador No. 80, Centro Universitario, CP 5500 Mendoza, Argentina

Received 11 October 2012; Accepted 19 December 2012

Academic Editor: Aldo Pende

Copyright © 2013 Nicolás F. Renna et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The objective of this work was to demonstrate the role of COX-2 enzyme at the vascular in experimental model of metabolic syndrome. SHR male WKY rats were employed; they were distributed in 8 groups ( each): control (W); W + L: WKY rats receiving 20 mg/kg of lumiracoxib by intraesophageal administration; SHR; SHR + L: SHR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Rats (FFR): WKY rats receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; FFR + L: FFR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Hypertensive Rats (FFHR): SHR receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; and FFHR + L: FFHR + 20 mg/kg of lumiracoxib by intraesophageal administration. Metabolic variables, blood pressure, morphometric variables, and oxidative stress variables were evaluated; also MMP-2 and MMP-9 (collagenases), VCAM-1, and NF-κB by Westernblot or IFI were evaluated. FFHR presented all variables of metabolic syndrome; there was also an increase in oxidative stress variables; vascular remodeling and left ventricular hypertrophy were evidenced along with a significant increase in the expression of the mentioned proinflammatory molecules and increased activity and expression of collagenase. Lumiracoxib was able to reverse vascular remodeling changes and inflammation, demonstrating the involvement of COX-2 in the pathophysiology of vascular remodeling in this experimental model.