线粒体靶向药MitoQ对病毒性心肌炎保护作用的相关研究

Study on the protective effect of MitoQ on viral myocarditis

目的:本研究旨在探讨线粒体靶向药MitoQ对柯萨奇B3病毒(Coxsackie virus B3, CVB3)诱导的病毒性心肌炎小鼠心肌损伤的保护作用。方法:购买雄性BALB/c小鼠并且将其分为对照组、CVB3组(模型组)、CVB3+MitoQ(2 mg/kg)组、CVB3+MitoQ(4 mg/kg)组、CVB3+MitoQ(8 mg/kg)组。HE染色观察心肌细胞损伤水平;Western blot检测凋亡相关蛋白(Bax、Bcl-2)的表达;氧化应激试剂盒检测ROS和SOD的水平;ELISA法检测小鼠血清中心肌损伤标志物肌钙蛋白I(Troponin I,cTnI)、B型脑钠肽(brain natriuretic peptide, BNP)以及炎症因子(TNF-α、IL-6)的水平。结果:与对照组比较,CVB3组细胞受损严重,凋亡相关蛋白表达增加,氧化应激损伤增加,心肌损伤标志物(cTnI、BNP)和炎性因子(TNF-α、IL-6)水平增加(P<0.05)。相对于CVB3组、CVB3+MitoQ组的心肌细胞受损改善,凋亡相关蛋白表达被抑制,氧化应激损伤减少,cTnI、BNP、TNF-α、IL-6水平降低(均P<0.05)。MitoQ对心肌损伤的改善作用随剂量依赖性增加。结论:MitoQ能够改善病毒性心肌炎小鼠心肌损伤,减少细胞凋亡和炎性因子水平。

Objective:The purpose of this study was to investigate the protective effect of MitoQ,a mitochondrial targeting drug,on myocardial injury in mice with coxsackie virus B3(CVB3)-induced viral myocarditis.Methods:Male BALB/c mice were purchased and divided into control group,CVB3 group(model group),CVB3+MitoQ(2 mg/kg)group,CVB3+MitoQ(4 mg/kg)group,and CVB3+MitoQ(8 mg/kg)group.HE staining was used to observe the level of myocardial cell injury;Western blot was used to detect the expression of apoptosis-related proteins(Bax,Bcl-2);The levels of ROS and SOD were detected by oxidative stress kit;Detection of serum troponin I(cTnI),brain natriuretic peptide(BNP)and inflammatory factor(TNF)in mice by ELISA-α、IL-6.Results:Compared with the control group,the CVB3 group had severe cell damage,increased expression of apoptosis-related protein,increased oxidative stress damage,myocardial injury markers(cTnI,BNP)and inflammatory factors(TNF-α、IL-6)level increased(P<0.05).Compared with CVB3 group and CVB3+MitoQ group,the myocardial cell damage improved,the expression of apoptosis-related protein was inhibited,the oxidative stress damage was reduced,and cTnI,BNP,TNF-α、The level of IL-6 decreased(all P<0.05).MitoQ improved myocardial injury in a dose-dependent manner.Conclusion:MitoQ can improve myocardial injury in mice with viral myocarditis,reduce cell apoptosis and inflammatory factor levels.