中文摘要：

目的：研究多肽药物汇利心康（HLXK）对慢性心衰模型大鼠心肌细胞凋亡的影响。方法：取大鼠随机分为正常对照组、模型组、阳性对照（灌胃氯沙坦钾6mg·kg-1,每日1次）组和HLXK低、中、高剂量（腹腔注射10、30、90μg·kg-1,每日2次）组,每组8只,后5组腹腔注射盐酸多柔比星（隔天给药,15d）建立慢性心衰模型,同时给予相应药物。10周后用高频彩超测定各组大鼠左心室收缩末期容积（LVESV）和射血分数（EF）,免疫组化法检测心肌组织中Bcl-2、Bax蛋白表达。结果：与正常对照组比较,模型组大鼠LVESV明显增加,EF明显减少（P〈0·01）,表明其心功能明显减退;且Bcl-2蛋白表达明显减弱,Bax蛋白表达明显增强（P〈0·01）。与模型组比较,阳性对照组和HLXK中、高剂量组LVESV明显减少,EF明显增加,Bax蛋白表达明显减弱,Bcl-2蛋白表达明显增强（P〈0·05或P〈0·01）;HLXK低剂量组仅Bax蛋白表达明显减弱,Bcl-2蛋白表达明显增强（P〈0·05）。结论：HLXK可能通过增强模型大鼠Bcl-2蛋白表达、抑制Bax蛋白表达,从而抑制心肌细胞凋亡。

英文摘要：

OBJECTIVE：To explore the effects of the polypeptide drug Huilixinkang（HLXK） on the myocardial apoptosis in rats with chronic heart failure（CHF）.METHODS：Rats were randomly divided into normal control group,model group,positive control group（intragastric administration of losartan 6 mg·kg-1,once a day） and HLXK low-dose,medium-dose and high-dose groups（intraperitoneal injection 10,30,90 μg·kg-1,twice a day） with 8 rats in each group.The latter 5 groups were given intraperitoneal injection of doxorubicin hydrochloride every 2 days for consecutive 15 days to establish CHF model and received relevant medicine.After 10 weeks of treatment,LVESV and EF of rats were measured by echocardiography,and expression of Bcl-2 and Bax in myocardial tissue were determined with immunohistochemistry technique.RESULTS：Compared with normal control group,LVESV of model group increased significantly,and EF decreased significantly（P〈0.01）,the heart function markedly reduced and the expression of Bcl-2 protein decreased and expression of Bax protein enhanced significantly（P〈0.01）.Compared with model group,LVESV level and expression of Bax protein in positive control group and HLXK medium-dose and high-dose groups decreased significantly while EF level and expression of Bcl-2 protein increased significantly（P〈0.05 or P〈0.01）.The expression of Bax protein in HLXK low-dose group decreased significantly,and the expression of Bcl-2 protein enhanced significantly（P〈0.05）.CONCLUSION：HLXK can inhibit myocardial apoptosis by enhancing the protein expression of Bcl-2 and inhibiting the protein expression of Bax.