Effect of Atorvastatin on Ischemia-reperfusion Myocardial Cell Apoptosis in Rats

Objective To observe the effect of short-term pretreatment with atorvastatin on ischemia-reperfusion myocardial cell apoptosis in rats,to investigate its possible mechanism.Methods A total of 48 male SD rats weighting 250～300 g were randomly divided into sham-operated group(group A,0.9% normal saline,2 ml/d),ischemia-reperfusion group(group B,0.9% normal saline,2 ml/d),atorvastatin group(group C,atorvastatin 20 mg·kg-1·d-1) and atorvastatin+N-nitro-L-arginine methyl ester(L-NAME)group(group D,atorvastatin 20 mg·kg-1·d-1,L-NAME 15 mg/kg).L-NAME was injected from tail vena 15 min before ischemia.After 3 days of pretreatment,rats were subjected to 30 min left-anterior-descending coronary artery occlusion and 120 min reperfusion.After reperfusion,serum nitric oxide(NO) levels,total superoxide dismutase(TSOD) vitality and malondialdehyde(MDA)of myocardial tissue were measured.The apoptotic morphological changes were observed by hoechst fluorescence staining,and the fas protein expression by immunohistochemistry and cardiomyocyte apoptosis index(AI) by llow cytometry.Results When compared with group B,atorvastatin increased NO content and TSOD vitality,decreased MDA content,depressed fas expression,and inhibited cardiomyocyte apoptosis(P0.01).In group D,NO decreased,MDA increased(P0.01),similar to group B(P0.05),decreased TSOD vitality decreased,fas expression and cardiomyocyte apoptosis increased as compared with group C(P0.01).Conclusion Atorvastatin can reduce ischemia reperfusion injury by inhibiting apoptosis of cardiacmyocyte.Its mechanism may be related to reduction of the production of oxygen derived free radicals and decrease of fas protein expression.NOS-NO may be one of the pathways to inhibit cardiacmyocyte apoptosis.