摘要
目的 观察新型免疫抑制剂FTY72 0对病毒性心肌炎 (VM)的保护作用 ,探讨其治疗VM的分子机制。方法 建立实验性VM模型。采用Westernblot法分别测定ERK1 / 2蛋白 ,磷酸化ERK1 / 2 (P ERK1 / 2 )的表达变化。结果 FTY72 0能明显减少柯萨奇B3病毒 (CVB3)感染后心肌酶释放 ,心肌细胞搏动较病毒感染组维持时间长 ,心肌细胞病变发展亦较缓慢 ,病毒滴度显著低于病毒感染组。而且感染CVB3后FTY 72 0治疗组的心肌细胞内P ERK1 / 2活性持续降低。结论 FTY72 0对CVB3病毒感染的乳鼠心肌细胞有明显的保护作用 ,它可以通过抑制ERK1 / 2信号通路使病毒复制能力降低 ,从而抑制CVB3基因的表达和复制。
Objective To observe the protective effect of FTY720 on rat cardiomyocytes infected with coxsackie B_3 virus (CVB_3) and its moleaular mechanism.Methods Establish an experimental model of viral myocarditis through the culture of cardiac cells of newborn SD rats.Western blot was used to study the protein of excellular regulated kinase(ERK) and Phospho-ERK in dexamethasone group and FTY720 group.Results FTY720 could inhibit the release of enzymes from myocardial cells which were infected by CVB_3 and decrease obviously the reproduction of virus in myocardial cells; and the protein of P-ERK in FTY720 group is lower than CVB_3 group(P<0.01)and dexamethasone group (P<0.05).Conclusion FTY720 had a significant protective effect in experimental myocarditis in vitro through ERK1/2 signaling pathway played.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2005年第3期220-222,i001,共4页
Journal of Applied Clinical Pediatrics
基金
卫生部科学研究基金资助 (98- 1 - 1 38)
