Atorvastatin inhibits Fas expression in ischemia-reperfusion induced myocardial cell injury

Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (i/r) injury. inhibition of fas expression prevents i/r induced apoptosis. however, the influence of atorvastatin on fas expression in i/r injurywas not studied. therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis andfas expression following acute i/r in vivo.methods: thirty wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (i/r)group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. apoptosis of the cardiomyocyteswas observed under electron microscopy and determined by optic microscopy with tunel (terminal deoxynucleotidyltransferase (tdt)-mediated dutp nick end-labeling) staining. to detect the expression of fas in thecardiomyocytes, immunohistochemistry method was used. image analysis system was used to quantitatively estimatethe positive metric substances of immunohistochemistry through the mean optic density.results: numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups andweren’t observed in the sham-operated group. fas expression was significantly higher in the ischemia-reperfusion groupas compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with i/rgroup.conclusion: upregulation of fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis,and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting fas expression.