Heart injury alleviated by erythropoietin and the relationship between cardiomyocyte apoptosis and p-Akt protein in rats with myocadial infarction

摘要

Objective: To investigate the protective effect of erythropoietin (EPO) on myocardial infarction in rats with cardiac injury and its mechanism. Methods: 60 healthy female Sprague Dawley rats aged 8 weeks were randomly divided into mock surgical (MS) group, myocardial infarction (MI) group and EPO group, with 20 in each group. 4 weeks after modeling, among the three groups of rats, the left ventricular ejection fraction (LVEF), fractional shuotening (FS), LDH and CK-MB expression of related biochemical indicators, infarct size, cardiomyocytes apoptosis, and the expression of p-Akt protein in myocardial tissues were detected. Among the myocardial infarction rats, the correlation between myocardial apoptosis index and p-Akt protein expression in myocardial tissues was analyzed. Results: The LVEF value, FS value, and expression of LDH and CK-MB in the MS group were better than those in MI and EPO group (P<0.05). The indicators in the EPO group were better than those in the MI group (P<0.05); the myocardial infarct size and cardiomyocyte apoptosis in the MS group were smaller than those in the MI group and the EPO group (P<0.05). However, the myocardial infarct size and cardiomyocyte apoptosis in the EPO group were lower than those in the MI group (P<0.05). The p-Akt protein in the MS group was higher than that in the MI group and EPO group. The p-Akt protein in the EPO group was increased than that in the MI group (P<0.05). Among the myocardial infarction rats, there was a negative correlation between myocardial apoptosis index and p-Akt protein expression in myocardial tissues (r=-0.623, P<0.05). Conclusion: For rats with myocardial infarction, EPO can effectively improve their cardiac function, and reduce myocardial infarct size and myocardial apoptosis. The mechanism of protective effect on cardiomyocytes may be relied on the regulation of Akt anti-apoptotic signaling pathway.