清心Ⅱ号抗病毒性心肌炎心肌凋亡和纤维化的效应及机制

The effect and mechanism of Qingxin Ⅱ in resisting the myocardial apoptosis and fibrosis

目的研究血浆AngⅡ与心肌c-myc在病毒性心肌炎心肌纤维化的作用及清心Ⅱ号的干预。方法建立病毒性心肌炎慢性期心肌纤维化模型后小鼠,随机分为模型组(n=10),卡托普利治疗组(n=17),清心Ⅱ号高、中、低剂量治疗组(每组n=17),另设正常组(n=10)。正常组和模型组给予生理盐水灌胃,治疗组分别给予卡托普利和清心Ⅱ号高中低剂量灌胃。疗程结束后分别采集心脏,应用放免法检测各组血浆AngⅡ含量;免疫组化技术检测心肌组织c-myc基因表产物,TUNEL法检测心肌细胞凋亡指数。结果清心Ⅱ号具有明显抗凋亡和抗心肌纤维化作用,其显抗凋亡和抗心肌纤维化作用具有剂量依赖性,抗心肌纤维化作用与卡托普利相当。结论血浆AngⅡ与心肌c-myc在病毒性心肌炎心肌纤维化形成过程中发挥重要作用,清心Ⅱ号具有抗心肌纤维化作用。

Objective To study The effect of the angiotensin Ⅱ and c-myc gene expressions of cardiac tissue in apoptosis of myocardial fibrosis in viral myocarditis and interference of Qingxin Ⅱ Recipe. Methods Mice with chronic viral myocarditis （VMC） were established by intraperitoneal injection and randomly divided into the model group （n = 10）, the captopril treatment group （n = 17） and the Qingxin Ⅱ treatment groups with high dose, middle dose, low dose （n = 17, respectively）. Another 10 mice were set as normal group. The normal and model groups were given normal saline, the captopril group was given eaptopril, and the Qingxin Ⅱ groups were given Qingxin Ⅱ from high to low dose respectively. After the treatment, The angiotensin Ⅱ levels of blood plasma were observed by radioimmunoassay （RIA）. The c-myc gene expressions of cardiac tissue were determined by immunohistochemical technology and cadiocyte apoptosis indexs were detected by TUNEL method. Results Qingxin Ⅱ had a distinct effect on the anti-apoptosis and the anti myocardial fibrosis. A dose dependent on anti-apoptosis and anti-myocardial fibrosis was observed. Qingxin Ⅱ had equally effect with captopril on anti myocardial fibrosis. Conclusions The angiotensin Ⅱ and c-myc gene has an influential role in the process of myocardial fibrosis in viral myocarditis and Qingxin Ⅱ has a good effect on the anti-virus and the anti-myocardial fibrosis.