摘要
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 a-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〈0.05 or 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.
出处
《中国分子心脏病学杂志》
CAS
2017年第6期2306-2311,共6页
Molecular Cardiology of China
基金
国家自然科学基金项目(81460066)
