Abstract:

Abstract:Objective To investigate the protective effect of  cardiomyopeptidin(CMP) for injection preconditioning on the immature myocardial ischemia-reperfusion injury in young rats,and clarify its mechanism.Methods 30 young healthy SD rats were randomly divided into sham-operated group,model control group and CMP　group (n=10).The levels of serum lactic dehydrogenase （LDH）,creatine kinase MB（CK-MB）,troponin Tn-T were detected;the contents of superoxide dismutase (SOD),malondialdehyde (MDA),nitric oxide(NO),total nitric oxide synthase (TNOS),inducible nitric oxide synthase (iNOS)and endothelial nitric oxide synthase（eNOS）in myocardium tissue were measured;the expression levels of iNOS,eNOS and Caspase-3 protein in myocardial tissue were detected by immunohistochemical method.The expressions of iNOS,eNOS and Caspase-3 mRNA  in myocardial tissue were mea
sured by real-time fluorescence quantitative PCR.The changes of myocardial structures were observed with optical microscope and transmission electron microscope.The apoptosis of myocytes was observed by TUNEL.Results Compared with model control group,the levels of LDH,CK-MB,Tn-T in CMP group were decreased(P< );Compared with sham-operated group,the contents of MDA,SOD,TNOS,and iNOS were increased and the expression levels of iNOS and caspase-3 mRNA were significantly down-regulated in CMP group,but less than those in model control group（P<0.01 or P<0.05）.Several pieces of myocardial hemorrhage and inflammatory cell infiltration were observed in model control group,severe degeneration and necrosis of myocytes could be found,the apoptotic myocytes were significantly increased;while in CMP group,the myocardial pathological injuries were mitigated,only mild degeneration and necrosis of myocardial cells could be found,the vascular structure was near-complete,the number of apoptotic myocytes between sham operation group and control group.Conclusion Cardiomyopeptidin for injection preconditioning can protect immature myocardium against ischemia-reperfusion injury in young rats.The mechanism may be associated with reducing oxygen free radical (OFR) and NO production,inhibiting the  expressions of iNOS mRNA,Caspase-3 mRNA and Caspase-3 protein in myocytes,and reducing apoptosis.

Key words: immature myocardium;cardiomyopeptidin;ischemia-reperfusion injury;ischemic preconditioning;apoptosis