Effects of pioglitazone on myocardial peroxisome proliferator-activated receptor gamma co-activator lα expression in rats with myocardial ischemia/reperfusion injury.
- Author:
Lin SHEN
1
;
Hao WANG
;
Ping YE
Author Information
- Publication Type:Journal Article
- MeSH: Anilides; pharmacology; Animals; Apoptosis; Male; Myocardial Reperfusion Injury; metabolism; Myocardium; metabolism; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Rats; Rats, Sprague-Dawley; Thiazolidinediones; pharmacology; Transcription Factors; antagonists & inhibitors; metabolism
- From: Journal of Southern Medical University 2014;34(2):197-200
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of pioglitazone on the expression of peroxisome proliferator-activated receptor gamma co-activator lα (PGC-lα) in rat myocardium following myocardial ischemia/reperfusion (I/R) injury.
METHODSTwenty-four SD rats were randomly divided into 4 equal groups, namely I/R group, pioglitazone (5 mg/kg daily) group, pioglitazone (10 mg/kg daily) group, and pioglitazone (10 mg/kg) +peroxisome proliferator-activated receptor γ (PPARγ)-specific antagonist GW9662 group. Myocardial I/R injury was induced by ligation of the left anterior descending coronary artery for 30 min and reperfusion for 120 min. Myocardial apoptosis following I/R injury was examined with TUNEL assay; RT-PCR and Western blotting were employed to detect the expression of PGC-lα mRNA and protein, respectively.
RESULTSPioglitazone treatment significantly suppressed myocardial apoptosis (21.4%∓8.8%,17.3%∓8.7%, 40.1%∓12.3%, P<0.05) following I/R injury and up-regulated myocardial PGC-lα expression at both the mRNA and protein levels (P<0.05), but these effects were antagonized by GW9662 (P<0.05).
CONCLUSIONPioglitazone can inhibit myocardial apoptosis induced by I/R injury and up-regulate myocardial PGC-lα expression, and these effects are mediated by PPARγ.
