Effect Of Shenmai Injection On Myocardial Ischemia/Reperfusion Injury In Rats

Objective :To investigate the Effect of Shenmai injection on myocardial ischemia/reperfusion injury in rats.Methods: 30 SD rats were randomly divided into three groups: sham group (operation group) , IR group (ischemia-reperfusion without any intervention), SM group (administered with Shenmai injection ),then 10ml·kg^-1 Shenmai injection were given in Shenmai group and the 0. 9% NaCl 10ml·kg^-1 were given in sham group and IR group for three days . After thoracotomy and ligation, the rats were injured by ischemia and relaxed 30 minutes later, then reperfusioned for 90 minutes ,the myocardial ischemia-reperfusion models in rats were established during the experiment. The PECAM-1 protein expressions were evaluated by FCM method, the ICAM-1 protein expressions were evaluated by immunohistochemistry, the contents of malondialdehyde (MDA) in serum were detected, The activities of superoxide dismutase ( SOD) in serum were measured.Results:Compared with sham group , the expressions of PECAM-1 in neutrophilic granulocytes and lymphocytes from blood in IR group were increased significantly, the expression levels of ICAM-1 protein in myocardium were increased significantly, the activities of SOD in serum were decreased significantly , the contents of MDA in serum were increased significantly .Compared with IR group, the expressions of PECAM-1 from blood in SM group were decreased, the expression levels of ICAM-1 protein in myocardium were decreased significantly, the activities of SOD in serum were increased significantly, the contents of MDA in serum were decreased significantly.Conclusion: These data suggest that:(l) The expressions of PECAM-1,ICAM-1 and MDA were increased significantly, the activities of SOD in serum were decreased significantly in ischemia-reperfused myocardium (MIR) rats.(2) Shenmai injection can greatly depressed expression of PECAM-1,ICAM-1and MDA, can greatly depressed the activities of SOD in serum.(3)Shenmai injection may protect myocardium ischemia/reperfusion injury, down-regulated expression of PECAM-1,ICAM-1,MOD and up-regulated activities of SOD may be the possible therapeutic mechanisms.