强心颗粒抑制慢性心力衰竭心气虚兼血瘀水肿证模型大鼠心肌细胞凋亡实验研究

Experimental Study of Qiangxin Granules Inhibiting Cardiomyocytes Apoptosis in Rat Model of Chronic Heart Failure with Heart Qi Deficiency,Blood Stasis and Edema Syndrome

目的 ：研究强心颗粒抑制慢性心力衰竭心气虚兼血瘀水肿证（HQD-BS-ES）大鼠心肌细胞凋亡的疗效及机制。方法 ：清洁级雄性SD大鼠80只,随机分为正常（Control）组20只、造模组60只,采用阿霉素（ADM）联合丙基硫氧嘧啶（PTU）双重因子攻击技术复制HQD-BS-ES大鼠模型,将存活成模大鼠随机分为模型（Model）组、缬沙坦（VAL）组、强心颗粒（QXP）组各18只。检测比较治疗后各组大鼠的生存率、LDH、ROS、MDA、SOD、心肌细胞凋亡水平以及Rac-1蛋白活化水平。结果：治疗后与正常组比较,模型组、缬沙坦组、强心颗粒组大鼠生存率、LDH、ROS、MDA、SOD、心肌细胞凋亡指数、Rac-1蛋白活化水平均有显著改变。与模型组比较,强心颗粒组大鼠生存率、LDH、ROS、MDA、SOD、心肌细胞凋亡指数、Rac-1蛋白活化水平均显著改善（均P〈0.05）。与缬沙坦组比较,强心颗粒组生存率、LDH无统计学意义,而ROS、MDA、SOD、心肌细胞凋亡指数、Rac-1蛋白活化水平均明显改善（均P〈0.05）。结论：强心颗粒具有很好的抑制氧化应激诱导的心肌细胞凋亡的能力,这可能是强心颗粒干预慢性心力衰竭HQD-BS-ES的重要机制之一。

Objective：To study the curative effect of Qiangxin granules（QXP） on inhibiting cardiomyocytes apoptosis of rats with chronic heart failure of heart qi deficiency complicated with blood stasis and edema syndrome（HQD-BS-ES）. Methods：Eighty SD rats were randomly divided to normal group（n= 20） and chronic heart failure of HQD-BS-ES group（n= 60） which was established by administering adriamycin plus propylthiouracil. And then the latter were randomly divided to 3 groups including model control group（n= 18）,valsartan（VAL） group（n= 18） and QXP group（n= 18）. The survival rate,lactate dehydrogenase（LDH）,reactive oxygen species（ROS）,malondialdehyde（MDA）,superoxide dismutase（SOD）,apoptosis index and Rac1 relative content were evaluated and compared. Results：Compared with the control group,the survival rate,LDH,ROS,MDA,SOD,apoptosis index and Rac1 relative content in other groups improved significantly（P0.05）. Compared with the model group,the survival rate,LDH,ROS,MDA,SOD,apoptosis index and Rac1 relative content of the QXP group improved significantly（P0.05）. Compared to VAL group,the survival rate and LDH of the QXP group showed no statistical difference,while the ROS,MDA,SOD,apoptosis index and Rac-1 relative content of the QXP group improved significantly（P0.05）. Conclusion：QXP has a good effect on inhibiting cardiomyocytes apoptosis induced by oxidative stress,which could be an important mechanism of QXP for curing chronic heart failure of HQD-BS-ES.