MAPK途径在病毒性心肌炎发病机制中的作用

MAPK pathway and the pathogenesis of viral myocarditis

目的研究丝裂原活化蛋白激酶(MAPK)途径在病毒性心肌炎(VMC)发病机制中的作用。方法应用嗜心性柯萨奇B3病毒Nancy株感染BALB/C小鼠,并于感染后第0、4和10天取小鼠心肌,做病理观察。同时在感染0、20、40、60和80 min后检测小鼠心肌细胞MAPK(磷酸化的ERK1/2、JNK、p38)通路的研究,观察细胞的凋亡情况。结果小鼠造模后经HE染色显微镜下观察,随着感染时间的增长,心肌细胞的损伤也更加明显,并在0、4和10天凋亡情况逐渐增加;磷酸化ERK1/2的表达量随着感染时间的增长而增加,磷酸化JNK在60、80 min时显著升高,差异有统计学意义(P<0.05)。ERK1/2下游蛋白rsk90的磷酸化情况也增加,差异有统计学意义(P<0.05)。结论在VMC过程中,通过ERK1/2途径刺激心肌产生炎性反应。

Objective Viral myocarditis（VMC）is a common cardiovascular disease in children, and its incidence is increasing year by year. Through the animal model, its pathogenesis was studied. Methods The BALB/C mouse was infected by myocarditic coxsackie virus B3. The myocardium samples were collected after infected for 0,4 and 10 days for pathological studies. And the myocardium samples were collected after infected for 0,20,40,60 and 80 min for the study of the MAPK pathway,and the apoptosis status was detected. Results The damage of myocardial cells was more obvious with the infected time increasing by HE staining. The ERK1/2 was increased with the time of infection. Its downstream protein,phosphorylation of rsk 90 was also increased. Conclusion In the process of VMC,the ERK1/2 pathway stimulated cardiac inflammatory response.