辛伐他汀对病毒性心肌炎小鼠心肌线粒体结构及酶活性的影响

目的:研究辛伐他汀对BALB/c小鼠病毒性心肌炎急性期心肌线粒体结构和酶活性的影响以及对病毒性心肌炎急性期的作用。方法:应用柯萨奇B3病毒制作BALB/c小鼠病毒性心肌炎模型,辛伐他汀混悬液灌胃,按辛伐他汀剂量不同分为1 mg/kg组、10 mg/kg组及100 mg/kg组,并设正常对照组及病毒感染对照组,7 d后观察心肌组织病理学改变,线粒体超微结构,线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性变化。结果:与感染对照组比较,辛伐他汀1 mg/kg组各检测指标无显著性改变(P>0.05),辛伐他汀10 mg/kg组及100 mg/kg组心肌线粒体结构破坏均减轻,线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性明显增高(均为P<0.01),心肌组织损伤程度亦明显减轻(P<0.05)。辛伐他汀100 mg/kg组心肌线粒体结构破坏较10 mg/kg组减轻,线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性进一步增高(P<0.05)。结论:辛伐他汀在有效剂量下对小鼠病毒性心肌炎急性期心肌线粒体结构和功能具有保护作用,这种保护作用可能是心肌细胞损伤减轻的重要原因。

Effect of Simvastatin on Myocardial Mitochondrial Structure and Activity of Adenosine Triphosphatase in Mice with Myocarditis

Objective: To explore changes of myocardial mitochondrial structure and activity of adenosine triphosphatase(ATPase) in mice with myocarditis,and observe the intervention effect of simvastatin.Methods: Sixty male BALB/c mice were divided into five groups randomly(n=12).Mice in viral control group,oral administration of simvastatin 1mg/kg group,10 mg/kg group,and 100 mg/kg group,were inoculated intrapritoneally with 0.2 ml of CVB3(Nancy strain).Normal control mice group were inoculated intrapritonealy with 0.2 ml Eagle's solution.All the mice were sacrificed on day 7.The activity of Na~( )-K~( )-ATPase and Ca~(2 )-ATPase of myocardial mitochondria as well as the morphological of myocardial mitochondria were detected.Results: Compared with viral control group,there were no significant changes in all indices observed in the 1 mg/kg simvastatin group(P>0.05);in the 10 mg/kg and 100 mg/kg simvastatin group,the activity of mitochondrial Na~( )-K~( )-ATPase and Ca~(2 )-ATPase significantly increased(P<0.01,respectively),the grade of myocardial necrosis was significantly decreased(P<0.05,respectively),and the structure of mitochondria changed distinctly.The level of Na~( )-K~( )-ATPase and Ca~(2 )-ATPase in 100 mg/kg group was significantly(P<0.05,respectively) higher than in 10 mg/kg group.Conclusion: Simvastatin could reduce the damage of mitochondrial structure and function,which might exert a protective effect in myocarditis mice infected by CVB3 in acute period.