促红细胞生成素对压力负荷过重小鼠心肌具有保护作用

Cardioprotective effects of recombinant human erythropoietin on pressure-overloaded hearts in mice

目的探讨促红细胞生成素(EPO)对压负荷过重引起的左心室重构是否具有保护作用。方法采用主动脉弓缩窄术(TAC)的方法建立小鼠模型,小鼠随机分为假手术组(Sham)、模型组(TAC-PBS)和治疗组(TAC-EPO)。术后8周,测定红细胞压积与左心室(LV)重量,苏木精-伊红染色测定心肌细胞的横截面积,马松染色与狼星红染色测定心肌间质纤维化的面积,TUNEL法检测心肌细胞凋亡,绘制小鼠生存曲线。结果与Sham相比,模型组和治疗组左心室重量均显著升高,给予EPO治疗后,红细胞压积明显增加(P<0.01),但是心肌细胞的横截面积无明显变化(P>0.05)。与模型组相比,EPO治疗可显著改善TAC小鼠生存率,减少心肌纤维化及TUNEL阳性心肌细胞数量(P<0.05)。结论EPO对压负荷过重引起的左心室重构和过早死亡具有保护作用。

Objective To investigate the protective effect of erythropoietin（EPO）on left ventricular remodeling induced by excessive pressure overload.Methods The mouse models were established by transverse aortic constriction（TAC）,and the mice were randomly divided into sham operation group（Sham）,model group（TAC-PBS）and treatment group（TAC-EPO）.At 8 weeks after operation,hematocrit and left ventricular（LV）weight was detected,and HE was used to determine the cross-sectional area of cardiac myocytes,Masson staining and Sirius red staining were used to determine the area of myocardial interstitial fibrosis,myocardial apoptosis was detected by TUNEL,and the survival curves of mice was finished.Results Compared with sham group,the left ventricular mass of mice in model group and treatment group was increased significantly,and hematocrit was increased significantly after treatment with EPO（P〈0.01）,but there was no significant change for myocardial cells（P〉0.05）.Compared with the model group,EPO treatment could significantly improve the survival rate of TAC mice,reduce the myocardial fibrosis and the number of TUNEL positive myocardial cells（P〈0.05）.Conclusion EPO has protective effect on left ventricular remodeling and premature death caused by stress overload.