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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2013-01-01
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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. |
format | Article |
id | doaj-art-3fbfe98a75124848a34ae23030a0d3c1 |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2013-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
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 |
work_keys_str_mv | AT nicolasfrenna roleofcox2invascularinflammationanexperimentalmodelofmetabolicsyndrome AT emilianordiez roleofcox2invascularinflammationanexperimentalmodelofmetabolicsyndrome AT carinalembo roleofcox2invascularinflammationanexperimentalmodelofmetabolicsyndrome AT robertommiatello roleofcox2invascularinflammationanexperimentalmodelofmetabolicsyndrome |