Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR-γ and UCP2

The present study aimed to investigate whether pretreatment with rosuvastatin (RS) can provide cardioprotection in a myocardial ischemia/reperfusion (MI/R) model. The protective effect of RS on myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury was also evaluated by upregulating peroxisome proliferator-activated receptor-γ (PPAR-γ). In the present study, MI/R model was established and activities of superoxide dismutase (SOD), lactate dehydrogenase (LDH), creatine kinase-muscle/brain (CK-MB), malondialdehyde (MDA), and troponin I/T were measured. The infarct size was measured using Evans blue staining and cell viability was measured by MTT assay. Reactive oxygen species (ROS) levels were assessed by flow cytometry. Caspase-9, cytochrome c (cyt c), mitochondrial uncoupling protein 2 (UCP2) and PPAR-γ expression levels were detected by reverse transcription-quantitative polymerase chain reaction and western blotting. The results indicated that RS increased SOD activity, and decreased LDH, CK-MB, MDA and troponin I/T activities. The effect of RS was reversed by atractyloside (ATR). RS inhibited myocardial infarct size, downregulated expression of caspase-9 and cyt c and upregulated expression of UCP2 and PPAR-γ by inhibiting ATR. Furthermore, the results indicated that RS promoted cardiomyocyte viability, inhibited LDH release, reduced ROS production, decreased expression of caspase-9 and cyt c, and increased expression of UCP2 and PPAR-γ following OGD/R damage. Therefore, the present study demonstrated that RS protects primary myocardial cells against OGD/R injury by regulating PPAR-γ and UCP2. RS may be a promising therapeutic agent for treatment of MI/R injury.