Effects of erythropoietin on apoptosis and expression of AKT in rats of chronic heart failure / 天津医药

ABSTRACT

Objective To investigate the effects of erythropoietin (EPO) on myocardial apoptosis and protein kinase B (AKT) expression in rats of chronic heart failure (CHF). Methods Thirty male adult SD rats were randomly divided into two groups, sham-operated (Sham) group (n=6) and model (Model) group (n=24). The abdominal aortic coarctation was used to build CHF model. Sixteen survived rats after operation were randomly divided into two groups including EPO group and con-trol (Control) group. EPO group was received 3 000 U/kg EPO intraperitoneal injection 3 times/week for 4 weeks, and Sham group and Control group were received same volume of normal saline. The echocardiography was used to evaluate cardiac function after 4 weeks, 8 weeks and 12 weeks of treatment. After 12 weeks, all rats were sacrificed after 24 h fasting. The cell morphology and myocardial apoptosis were observed, and apoptosis index (AI) was calculated. Myocardial P-AKT/AKT pro-tein expression was detected by Western blot assay. Results Echocardiography showed that ventricular hypertrophy was found in model group after four weeks, heart failure 8 weeks. Compared with Control group, left ventricular ejection fraction (LVEF) was significantly higher after EPO intervention for 4 weeks (P < 0.05), systolic interventricular septum thickness (IVSs), end-systolic left ventricular posterior wall thickness (LVPWs), diastolic interventricular septum thickness (IVSd), af-ter left ventricular end-diastolic wall thickness (LVPWd) were significantly lower (P<0.05). The value of AI was significant-ly lower in EPO group than that of Control group (23.87%±1.45%vs 35.58%±2.81%, P<0.01). The OD value of P-AKT/AKT was significantly decreased in Control group (0.35±0.06) than that of Sham group (0.81±0.17), the value was significant-ly increased in EPO group (1.61±0.16) than that of Control group (P<0.01). Conclusion EPO can improve heart function, inhibit myocardial apoptosis,and promote pro-phosphorylation of AKT in rats with chronic heart failure.