论文部分内容阅读
目的 本文旨在研究FTY720对CVB3诱导的病毒性心肌炎细胞和动物模型的治疗作用.方法 利用CVB3病毒、乳鼠心肌细胞及小鼠建立病毒性心肌炎细胞和动物模型.通过观察心肌细胞病变情况、动物死亡率及心脏脏器系数、心肌组织HE染色及动物模型外周血清中LDH、CK-MB水平对FTY720的疗效进行评价.通过FTY720抑制病毒增殖实验及心肌细胞凋亡实验研究FTY720抗病毒性心肌炎的作用机制.结果 FTY720能够显著的抑制由CVB3引起的细胞病变(P＜0.05),显著的降低小鼠外周血中心肌酶LDH和CK-MB的水平及小鼠心脏脏器系数(P＜0.05),而对小鼠死亡率影响不大(P＞0.05).FTY720能够显著的抑制CVB3的增殖和心肌细胞的凋亡(P＜0.05或P＜0.01).结论 FTY720对CVB3诱导的病毒性心肌炎细胞和动物模型均具有一定的保护作用,其作用机制与抑制病毒增殖及心肌细胞凋亡有关.“,”Objective To investigate the protective effect and mechanism of FTY720 on CVB3 induced-myocardity.Methods The cell and mice models of CVB3 induced-myocardity was treated by FTY720.Protective effect on myocardity were detected by CPE,mice mortality,the level of LDH and CK-MB in Peripheral blood,HE and α-actin staining of myocardium and tissue.Inhibit effect of FTY720 on multiplication of CVB3 and B-lymphcyte,myocardial apoptosis were detected to study mechanism of FTY720.Results The CPE of myocardial cell were inhibited significantly(P＜0.05).The level of LDH and CK-MB in Peripheral blood of mice were decreased significantly(P＜0.05).Comparing with model groups,FTY720 could inhibit multiplication of CVB3 and myocardial apoptosis significantly(P＜0.05or P＜0.01).Conclusion Our study shown that FTY720 has protective effect of animal and cell models of myocarditis,which perhaps were realized by inhabiting multiplication of CVB3 and B-lymphcyte,myocardial apoptosis.