[Atorvastatin inhibits cardiomyocyte apoptosis via down-cegulation the expression mitofusin 2 after myocardial ischemia/reperfusion injury in rats].

OBJECTIVE: To investigate the effects of atorvastatin (statin for short) on cell apoptosis and the expression of mitofusin 2 (Mfn2) after myocardial ischemia/reperfusion (I/R) injury in rats. METHODS: A total of 32 male Sprague-Dawley rats were randomly divided into sham group, I/R group, statin group 1 and group 2, with 8 rats in each group. The rats in the two statin groups were given atorvastatin 10 and 40 mg/(kg.d) daily since the 7th day before I/R injury, respectively. The rats in the I/R group were given distilled water instead. The I/R injury models were induced by the ligation of left anterior descending (LAD) artery for 30 minutes followed by recovering the blood stream. Three hours after reperfusion, the I/R injured areas of rat hearts were harvested, and cardiomyocyte apoptosis was assessed by in situ terminal deoxynucleotidyl transferase (TdT)-dUTP nick-end labeling (TUNEL). Immunohistochemistry and Western blotting were respectively performed to determine the expressions of Mfn2 and phosphorylated Akt (p-Akt). RESULTS: Three hours after reperfusion, the cardiomyocyte apoptosis and Mfn2 protein expression of the I/R and statin treatment groups remarkably increased, and p-Akt expression significantly decreased (P<0.01) as compared with those of the sham group. Compared with those of the I/R group, cardiomyocyte apoptosis and Mfn2 protein expression of statin groups were significantly reduced in a slightly dose-dependent manner (P<0.05), and p-Akt expression was obviously raised (P<0.05). CONCLUSION: Atorvastatin can suppress cardiomyocyte apoptosis after I/R injury in rats, which may be related to the down-regulated expression of Mfn2.