2009Journal of Clinical CardiologyRequires access

Effect of erythropoietin on myocardial ischemia-reperfusion injury in rats

Wang Yuegang

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Abstract

Objective:To observe the effect of erythropoietin(EPO) on myocardial-reperfusion injury in rats,discuss the mechanism involved.Method:The left anterior descending branch of coronary artery (LAD) of rats was ligated for 30 min and then loosed for 3 h to establish ischemia/reperfusion heart model. 45 SD rats were randomly divided into 5 groups:Sham operation group (group SHAM),and 4 experimental groups:group IR,group LY,group EPO and group EPO+LY. The arrhythmias were monitored during experiment,to score the ventricular arrhythmias. The change of cardiac ultrastructure were examed by transmission electron microscope. Myocardia1 cells apoptosis were estimated by in situ nick end 1abeling (TUNEL)method. The levels of serum CK-MB and cTnI were detected. Result: EPO treatment decreased the arrhythmia score(P0.05),protected the ultrastructure of myocardium,decreased apoptotic index(P0.01),decreased the levels of serum CK-MB and cTnI(P0.01). LY294002 attenuated the effect of EPO. Conclusion:EPO treatment prevented against myocardial ischemia-reperfusion injury in rats,the cardioprotection by EPO required the PI3K pathway.

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Objective:To observe the effect of erythropoietin(EPO) on myocardial-reperfusion injury in rats,discuss the mechanism involved.Method:The left anterior descending branch of coronary artery (LAD) of rats was ligated for 30 min and then loosed for 3 h to establish ischemia/reperfusion heart model. 45 SD rats were randomly divided into 5 groups:Sham operation group (group SHAM),and 4 experimental groups:group IR,group LY,group EPO and group EPO+LY. The arrhythmias were monitored during experiment,to score the ventricular arrhythmias. The change of cardiac ultrastructure were examed by transmission electron microscope. Myocardia1 cells apoptosis were estimated by in situ nick end 1abeling (TUNEL)method. The levels of serum CK-MB and cTnI were detected. Result: EPO treatment decreased the arrhythmia score(P0.05),protected the ultrastructure of myocardium,decreased apoptotic index(P0.01),decreased the levels of serum CK-MB and cTnI(P0.01). LY294002 attenuated the effect of EPO. Conclusion:EPO treatment prevented against myocardial ischemia-reperfusion injury in rats,the cardioprotection by EPO required the PI3K pathway.

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Available abstract

Objective:To observe the effect of erythropoietin(EPO) on myocardial-reperfusion injury in rats,discuss the mechanism involved.Method:The left anterior descending branch of coronary artery (LAD) of rats was ligated for 30 min and then loosed for 3 h to establish ischemia/reperfusion heart model. 45 SD rats were randomly divided into 5 groups:Sham operation group (group SHAM),and 4 experimental groups:group IR,group LY,group EPO and group EPO+LY. The arrhythmias were monitored during experiment,to score the ventricular arrhythmias. The change of cardiac ultrastructure were examed by transmission electron microscope. Myocardia1 cells apoptosis were estimated by in situ nick end 1abeling (TUNEL)method. The levels of serum CK-MB and cTnI were detected. Result: EPO treatment decreased the arrhythmia score(P0.05),protected the ultrastructure of myocardium,decreased apoptotic index(P0.01),decreased the levels of serum CK-MB and cTnI(P0.01). LY294002 attenuated the effect of EPO. Conclusion:EPO treatment prevented against myocardial ischemia-reperfusion injury in rats,the cardioprotection by EPO required the PI3K pathway.

Key concepts: Medicine, Erythropoietin, Cardioprotection, TUNEL assay, Reperfusion injury, Troponin I, Ischemia, Internal medicine

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