黄芪总黄酮通过抑制内质网应激对小鼠病毒性心肌炎保护作用的实验研究  

The protective effects of total flavonoids of astragalus on inhibition of endoplasmic reticulum stress in murine model with coxsackie virus B3-induced acute viral myocarditis

作　　者：牛晓峰[1] 赵雅君[1] 陶谢鑫 黄侠[1] 柴花 赵明[1] 

机构地区：[1]内蒙古民族大学附属医院心内科,内蒙古通辽028000

出　　处：《临床心血管病杂志》2015年第2期129-132,共4页Journal of Clinical Cardiology

基　　金：内蒙古自治区科技厅资助项目(No:2011BS1101)

摘　　要：目的:探讨黄芪总黄酮对病毒性心肌炎小鼠心肌细胞内质网应激凋亡的作用。方法:将60只雄性Balb/c小鼠均分为病毒性心肌炎组、正常组及黄芪总黄酮组。病毒性心肌炎组与黄芪总黄酮组腹腔内无菌注射含0.1ml 10-9 50TCIDCVB3,正常组不注射CVB3病毒。黄芪总黄酮组小鼠每日腹腔注射20mg·L-1黄芪总黄酮0.2ml,观察小鼠的一般情况,7d时行血流动力学检查后处死取心脏标本,用TUNEL法检测各组小鼠心肌细胞凋亡情况,RT-PCR检测各组小鼠心肌细胞内质网伴侣蛋白GRP78和GRP94的mRNA表达水平。结果:1与正常组相比,病毒性心肌炎组小鼠血流动力学指标明显降低(P<0.05);与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠血流动力学指标有显著改善(P<0.05)。2TUNEL染色显示,与正常组相比,病毒性心肌炎组小鼠心肌细胞凋亡明显增多(P<0.05);与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠心肌细胞凋亡显著减少(P<0.05)。3与正常组相比,病毒性心肌炎组小鼠内质网伴侣蛋白GRP78和GRP94的mRNA表达水平均明显升高(均P<0.05),且其变化趋势与心肌细胞凋亡数相似;与病毒性心肌炎组小鼠相比,黄芪总黄酮组小鼠内质网伴侣蛋白GRP78和GRP94的mRNA表达水平明显下降(均P<0.05)。结论:黄芪总黄酮对病毒性心肌炎心力衰竭小鼠内质网应激介导的心肌细胞凋亡有保护作用,这可能是黄芪总黄酮改善病毒性心肌炎心力衰竭小鼠血流动力学的作用机制之一。Objective：To study the effects of total flavonoids ofastragalus （TFA） on cardiac myocyte apoptosis induced by endoplasmic retieulum stress in murine model with coxsackie virus B3-induced acute viral myocarditis. Method：Sixty Balb/c mice were divided into viral myocarditis group, normal control group and TFA group （n= 20）. Mice in viral group and TFA group intraperitoneally injected with 0.1 mol1^-9 50TCIDCVB3. TFA group peritoneally injected with 0.2 ml TFA （20 mg· L-1） everyday. After 7 days, hemodynamic examination was car- ried out, heart specimens were collected. The myocardial apoptosis was determined by TUNEL, the expression levels of GRP78 and GRP94 mRNA were detected by RT-PCR. Result：①Compared with normal control group, the indicators of hemodynamics in viral myocarditis group were significantly reduced （P〈0.01） ;compared with vi ral myoearditis group, the hemodynamics in TFA group was significantly improved （P〈0.05）. ②TUNEL stai- ning showed that myocardial apoptosis in viral myocarditisgroup was significantly increased （P〈0.01）, while sig- nificantly reduced in TFA group （P〈0. 05）. ③Compared with normal control group, the expression levels of GRP78 and GRP94 mRNA in viral myocarditis group were significantly higher （P〈0.01）, and the tendency was similar to the change of cell apoptosis. The levels of expression GRP78 and GRP94 mRNA in TFA group was sig- nificantly decreased compared with viral myocarditis group （P〈0.01）. Conclusion：TFA could protect myocardial apoptosis induced by endoplasmic reticulum stress in mice with viral myocarditis.

关 键 词：病毒性心肌炎 黄芪总黄酮 内质网应激 凋亡 

分 类 号：R331.3[医药卫生—人体生理学]