| Background and objectives:Myocardial ischemia reperfusion (I-R) injury continues to occur after cardiac operations that have been performed in a technically adequate manner. This injury contributes significantly to postoperative morbidity and mortality, despite meticulous adherence to presently known principles of myocardial protection. Myocardial hypertrophy caused by overload pressure was generally in clinical. Hypertrophic myocardium had different properties. Ischemia reperfusion injury was more serious in hypertrophic myocardium than in normal myocardium. Special myocardial protective methods should be used in order to get more protective effect in hypertrophic myocardium.Peroxisome proliferator-activated receptor-γ(PPAR-γ) is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily. PPAR-γregulates gene expression by forming a heterodimer with the retinoid X receptor (RXR) before binding to sequence-specific PPAR response elements (PPREs) in the promoter region of target genes, thereby regulating several metabolic pathways, including lipid biosynthesis and glucose metabolism. Thiazolidinediones (TZDs, i.e. rosiglitazone, pioglitazone), which are synthetic PPAR-γagonists, act as insulin sensitizers and are used in the treatment of type 2 diabetes. In the last few years, it has, however, become evident that the therapeutic effects of PPAR-γligands reach far beyond their use as insulin sensitizers. Recently, PPAR-γhas been implicated as a regulator of cellular inflammatory and ischemic responses. PPAR-γagonists may exert their anti-inflammatory effects by negatively regulating the expression of pro-inflammatory genes induced during macrophage differentiation and activation, by either PPAR-γdependent or independent mechanisms. Several lines of evidence suggest that TZDs protect the heart and other organs against the tissue injury caused by ischemia-reperfusion (I-R) injury and shock. The aim of this study...
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