EPO对阿霉素所致心衰大鼠氧化应激能力及细胞凋亡水平的影响

目的评价红细胞生成素（EPO）对阿霉素所致心力衰竭大鼠氧化应激和细胞凋亡水平的影响，并探讨其抗心力衰竭的可能机制。方法30只SD大鼠随机分为EPO组、心衰组和对照组（予相同体积生理盐水），每组10只。采用腹腔注射盐酸阿霉素（ADR）建立心衰大鼠模型，EPO组每日给予EPO50U·kg-1；心衰组每日给予相同体积生理盐水，观察10周。第11周行心脏超声检测并测定大鼠血清中超氧化物歧化酶（SOD）、丙二醛（MDA）水平及心肌组织中FasmRNA的表达，Tunel法测心肌细胞凋亡。结果与心衰组相比，EPO组左室射血分数显著提高、MDA及FasmRNA的水平降低、心肌细胞凋亡指数（AI）减少、SOD活力增加（均P〈0．01）；与对照组相比，心衰组大鼠SOD活力下降、MDA水平升高、FasmRNA的表达及心肌细胞AI指数增加（均P〈0．01）。结论EPO能显著减轻阿霉素诱导的血流动力学障碍、改善心功能，且此作用可能与氧化应激能力及细胞凋亡水平降低有关。

Effect of Erythropoietin on Oxidative Stress and Myocardial Apoptosis in Rat with Adriamycin-induced Heart Failure

Objective To investigate the effect of erythropoietin （EPO） on oxidative stress and myocardial apoptosis in rat with adriamycin-induced heart failure and to explore its possible mechanism. Methods 30 SD rats were randomly divided into three groups：EPO group, heart failure group and control group,recived a equivalent with 10 rats in each group. The heart failure model was established by intraperitoneal injection of adriamyein. In EPO group, rats reeived erythropoietin （50 U .kg-1） everyday for five weeks,while in heart failure group, rats recived a equivalent volume of saline daily. After 10 weeks of remedy, the echocardiography was performed in the eleventh week and superoxide dismutase （SOD） activity,malondialdehyde （MDA） concentration and the expression of Fas mRNA were detected, and myocardial apoptosis was assessed by using TUNEL method. Results Compared with heart failure group, EPO significantly improved left ventrieular ejection fraction,enhanced the activity of SOD （P〈0.01）, decreased the content of MDA and the expression of Fas mRNA, and reduced myocardial apoptosis. Compared with control group, SOD activity was significantly decreased, and MDA content, Fas mRNA expression and myocardial apoptosis were significantly increased in heart failure group （P〈0. 01）. Conclusion EPO may relieve adriamycin-induced hemodynamic abnormality and improve cardiac function involving the improvement of oxygen stress and decrease of apoptosis in cardiac myocytes.