黄芪甲甙对病毒性心肌炎小鼠心肌组织蛋白酶L表达的作用

目的探讨黄芪活性成分黄芪甲甙对病毒性心肌炎(VMC)小鼠心肌中组织蛋白酶L(cathepsinL,CL)表达的作用。方法BALB/C小鼠100只,随机分成6组。非感染小鼠腹腔无菌注射病毒培养液,分为正常对照组(A组10只,以羧甲基纤维素钠0.1ml灌胃7d)、9%黄芪甲甙对照组(B组10只,9%黄芪甲甙0.1ml灌胃7d);余80只小鼠以柯萨奇病毒(CVB3)腹腔无菌注射制作VMC模型,VMC小鼠随机分为心肌炎对照组和1%、3%、9%黄芪甲甙干预心肌炎组,分别以羧甲基纤维素钠及1%、3%、9%黄芪甲甙0.1ml灌胃7d(分别为C、D、E、F组,每组20只)。14d后处死全部小鼠并取其心脏。采用RT_PCR和免疫组化半定量检测心肌CLmRNA及蛋白表达水平。结果F组小鼠较C组死亡率明显降低10%(2/20例)vs45%(9/20例),χ2=6.14,P<0.05],B组无小鼠死亡;与C组相比,CLmRNA、蛋白表达水平以及心肌病变积分在F组均显著下降,而1%、3%黄芪甲甙对心肌炎小鼠CLmRNA、蛋白表达及心肌病变积分无明显影响。结论黄芪甲甙可能通过抑制cathepsinL表达,对BALB/C小鼠CVB3心肌炎具有良好的治疗作用。

Effect of astragaloside on the expression of cathepsin L in the myocardium with viral myocarditis

Objective To investigate the effect of astragaloside,one of the active components of astragalus monosome,on myocardial cathepsin L (CL)expression in murine model of coxsackievirus B (CVB3)myocarditis. Methods One hundred BALB/C mice were randomly divided into 6 groups. Group A (n=10,treated with CMC 0.1 ml intragastric injection for 1 week)was served as normal control and group B(n=10,treated with 9%astragaloside 0.1 ml ig for 1 week)as treatment control. The eighty infected animals treated with CMC and 1%,3%,9%astragaloside 0.1 ml ig for 1 week(n=20 in each group)were served as group C,D,E,F,respectively. The mice were killed 14 days later and their hearts were removed for analysis. The levels of CL mRNA expression and protein in the myocardium were examined by RT-PCR and immunohistochemistry,respectively. Results The mortality was 10%(2/20)in 9%astragaloside treated infected animals (group F),which significantly reduced as compared to 45%(9/20)in group C (P<0.05).In uninfected animals,9%astragaloside did not cause any death. The levels of CL mRNA expression,protein and myocardial histopathologic scores in group F were significantly lower than those in group C. However,the CL expression and myocardial histopathologic scores were not influenced by 1%and 3%astragaloside. Conclusions Astragaloside may play a pivotal role in protecting the heart injury in BALB/C mice with CVB3 myocarditis by suppressing excessive expression of cathepsin L.