Effect of Rosiglitazone on Myocardial Ischemia-Reperfusion Injury in Rat Heart.
- Author:
Ki Chan HA
1
Author Information
1. Department of Pharmacology & Institute of Cardiovascular Research, Chonbuk National University Medical School, Jeonju 560-182, Korea. omphalos@chonbuk.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Peroxisome proliferator-activated-receptor-gamma;
Rosiglitazone;
Ischemia-reperfusion;
Lipid peroxidation;
Superoxide dismutase;
Catalase
- MeSH:
Animals;
Catalase;
Glutathione;
Heart*;
Hemodynamics;
Ischemia;
Lipid Peroxidation;
Peroxisomes;
Rats*;
Reperfusion;
Reperfusion Injury*;
Superoxide Dismutase
- From:The Korean Journal of Physiology and Pharmacology
2006;10(4):181-186
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study was undertaken to evaluate whether peroxisome proliferator-activated-receptor-gamma (PPAR-gamma) agonist-rosiglitazone (ROSI) induces postischemic functional recovery in Langendorf heart model. Hearts isolated from normal rats were subjected to 20 min of normoxia or 25 min zero-flow ischemia followed by 50 min reperfusion. In this acute protocol, ROSI (20 microgram/ml) administered 10 min before ischemia had no effect on hemodynamic cardiac function, but had protective effect on lipid peroxidation in in vitro experiments. In chronic protocol in which ROSI was given by daily gavage (4 mg/kg) for three consecutive days, ROSI could not prevent the hemodynamic alteration on cardiac performance, but has protective effect on the activity of superoxide dismutase (SOD). There was no significant difference in the contents of reduced glutathione (GSH) and catalase activity between ischemia-reperfusion (IR) and ROSI treated IR hearts. Although ROSI had no effect on hemodynamic factor, it had effect on antioxidant activity. Our results indicate that ROSI provides partial beneficial effects by inhibiting lipid peroxidation and/or recovering normal level of SOD activity in the ischemic reperfused heart.
