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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 To investigate the role of mitogen-activated protein kinase (MAPK) pathway in the pathogenesis of viral myocarditis (VMC). Methods BALB / C mice were infected with the co-infected Coxsackie virus B3 (NCBI) Nancy strain. The myocardium of mice were sacrificed on days 0, 4 and 10 after infection. At the same time, the pathways of MAPK (phosphorylated ERK1 / 2, JNK, p38) in mouse cardiomyocytes were detected at 0, 20, 40, 60 and 80 min after infection to observe the cell apoptosis. Results After modeling, the cells were observed under HE staining. The damage of cardiomyocytes became more obvious with the increase of infection time, and the apoptosis increased gradually at 0, 4 and 10 days. The expression of phosphorylated ERK1 / 2 With the increase of infection time, the phosphorylation of JNK increased significantly at 60 and 80 min, the difference was statistically significant (P <0.05). The phosphorylation of ERK1 / 2 downstream protein rsk90 also increased, the difference was statistically significant (P <0.05). Conclusions In VMC, inflammatory responses are stimulated by ERK1 / 2 pathway.