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目的:观察病毒性心肌炎(viral myocarditis,VMC)急性期心肌细胞p38MAPK信号通路的动态变化并探讨其可能的作用机制。方法:75只清洁级近交系4～6周龄雄性Balb/C小鼠,随机分为2组,心肌炎组60只,观察各时间点(第1、3、7和14天)心肌细胞磷酸化p38MAPK含量、心肌组织病理学改变及血清cTn-I水平的动态变化。对照组15只作总体对照。结果:病毒接种后第1天即出现心肌细胞p38MAPK明显活化,第3天达高峰,后渐降至对照组水平;这一变化早于炎症细胞浸润及血清cTn-I升高。结论:急性VMC早期存在p38MAPK信号通路活化,提示p38MAPK信号通路可能参与VMC的发病。
Objective: To observe the dynamic changes of p38 MAPK pathway in acute myocardium of viral myocarditis (VMC) and to explore its possible mechanism. Methods: Seventy-five male BALB / C mice aged 4 to 6 weeks were randomly divided into 2 groups and 60 in myocarditis group. The changes of phosphorylation of myocardial cells at each time point (days 1, 3, 7 and 14) P38MAPK content, myocardial histopathological changes and serum cTn-I levels of dynamic changes. Control group 15 only as an overall control. Results: On the first day after virus inoculation, the p38MAPK of cardiomyocytes was obviously activated, peaked on the third day and then decreased to the level of the control group. The change was earlier than that of inflammatory cell infiltration and serum cTn-I. Conclusion: The activation of p38 MAPK signaling pathway in acute VMC early suggests that p38 MAPK signaling pathway may be involved in the pathogenesis of VMC.