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

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 (n=8 each): control (W); W + L: WKY rats receiving 20 mg/kg of lumiracoxib by intraesophageal adminis...

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Main Authors: Nicolás F. Renna, Emiliano R. Diez, Carina Lembo, Roberto M. Miatello
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2013/513251
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author Nicolás F. Renna
Emiliano R. Diez
Carina Lembo
Roberto M. Miatello
author_facet Nicolás F. Renna
Emiliano R. Diez
Carina Lembo
Roberto M. Miatello
author_sort Nicolás F. Renna
collection DOAJ
description 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 (n=8 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.
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spelling doaj-art-3fbfe98a75124848a34ae23030a0d3c12025-02-03T01:07:28ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/513251513251Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic SyndromeNicolás F. Renna0Emiliano R. Diez1Carina Lembo2Roberto M. Miatello3Department of Pathology, School of Medicine, National University of Cuyo, Avenida Libertador No. 80, Centro Universitario, CP 5500 Mendoza, ArgentinaInstitute of Experimental Medicine and Biology of Cuyo (IMBECU)-CONICET, Mendoza, ArgentinaInstitute of Experimental Medicine and Biology of Cuyo (IMBECU)-CONICET, Mendoza, ArgentinaDepartment of Pathology, School of Medicine, National University of Cuyo, Avenida Libertador No. 80, Centro Universitario, CP 5500 Mendoza, ArgentinaThe 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 (n=8 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.http://dx.doi.org/10.1155/2013/513251
spellingShingle Nicolás F. Renna
Emiliano R. Diez
Carina Lembo
Roberto M. Miatello
Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
Mediators of Inflammation
title Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
title_full Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
title_fullStr Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
title_full_unstemmed Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
title_short Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome
title_sort role of cox 2 in vascular inflammation an experimental model of metabolic syndrome
url http://dx.doi.org/10.1155/2013/513251
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AT robertommiatello roleofcox2invascularinflammationanexperimentalmodelofmetabolicsyndrome