摘要
目的:探讨病毒性心肌炎心力衰竭小鼠心肌组织内质网应激介导的凋亡途径。方法:40只雄性Balb/c小鼠分为病毒性心肌炎组和正常对照组(n=20),病毒性心肌炎组应用柯萨奇B3病毒制作BALB/c小鼠病毒性心肌炎模型,观察小鼠的一般情况,7 d行血流动力学检查后处死取心脏标本,用TUNEL法检测心肌细胞凋亡,RTPCR检测心肌细胞内质网伴侣蛋白葡萄糖调节蛋白(GRP)78和GRP94的mRNA表达水平。结果:1与正常对照组相比,病毒性心肌炎组小鼠血流动力学指标明显降低(P<0.01);2TUNEL染色显示病毒性心肌炎心力衰竭小鼠心肌组织凋亡明显增多(P<0.01);3病毒性心肌炎组小鼠内质网伴侣蛋白GRP78和GRP94的mRNA表达水平均明显高于对照组(P<0.01)。结论:病毒性心肌炎心力衰竭小鼠内质网应激可能介导了心肌细胞凋亡。
Objective： To explore the apoptotic pathway mediated by endoplasmic reticulum stress in the mouse myocardium with heart failure induced by acute viral myocarditis caused by B-3 Coxsackie virus. Methods： Forty BALB/c male mice were randomly divided into 2 groups（ n = 20） ： the control group and the virus infection group, The BALB/e mouse myocarditis was induced by B-3 Coxsaekie virus and the mouse behavior was observed conventionally. All the mice were sacrificed on day 7 and the changes of left ventrieular pressure （LVP） and the rate of change of left ventricular pressure （LV dp/dt） were measured. The eardiomyocytie apoptesis was analyzed by TUNEL method and the mRNA expression level of endoplasmie retieulum haperones glucose-regulated protein（GRP）78 and GRP94 was detected by RT-PCR. Results： ①Compared with those of control group, the parameters of cardiac hemodynamies in the virus infection group were significantly decreased（ P 〈 0.01 ）; ②Compared with that of control group, myocardial apoptesis was significantly increased in the myocardial cells from mice with heart failure induced by acute viral myocarditis （ P 〈 0.01 ） ; ③The rnRNA expression level of GRP78 and GRP94 were increased significantly in the virus infection group compared with the control group. Conclusion： These findings suggest the endoplasmie retieulum stress may mediate the apoptosis of myocardial cells in the mice myocardium of heart failure induced by acute viral myocarditis caused by B-3 Coxsackie virus.
出处
《中国应用生理学杂志》
CAS
CSCD
2014年第5期461-464,共4页
Chinese Journal of Applied Physiology
基金
内蒙古自治区科技厅资助项目(2014MS0831)
关键词
病毒性心肌炎
心力衰竭
内质网应激
凋亡
viral myocardifis
heart failure
endoplasmic reticulum stress
apoptosis
