中药金叶败毒制剂抑制巨细胞病毒感染ERK／MAPK信号通路的研究  

The effect of Jinyebaidu on inhibition of extracellular signal regulated kinase 1 and 2 (ERK1/2) signaling pathway with human cytomegalovirus infection

作　　者：张宏秀[1] 闻良珍[1] 凌霞珍[1] 陈素华[1] 曾万江[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院妇产科,武汉430030

出　　处：《现代生物医学进展》2006年第11期1-3,共3页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(30271673);湖北省自然科学基金项目(2002AB132)

摘　　要：目的:通过对感染丝裂素活化蛋白激酶(Mitogen-Activated Protein Kinase,MAPK)细胞外信号调节激酶(extracellular signal-regulated kinase包括ERK1和ERK2)的信号通路的抑制作用,研究中药金叶败毒制剂治疗巨细胞病毒(human cytomegalovirus,HCMV)感染的分子机制。方法:使用免疫印记技术检测中药金叶败毒制剂和更昔洛韦(ganciclovir,GCV)干预HCMV感染的人胚肺成纤维细胞(human embryonic lung,HEL)的ERK表达水平,并观察MEK(mitogen-activated protein kinase kinase)特异性抑制剂PD 98059,中药金叶败毒制剂对细胞的病变作用(cytopathic effect,CPE)的影响。结果:两种药物都可抑制HCMV在HEL中的增殖,以PD 98059与中药金叶败毒制剂合用效果明显。中药金叶败毒制剂使磷酸化ERK1／2表达降低,对ERK1的抑制作用在感染后10min出现,30min达到高峰,对ERK2的抑制作用在感染后10min出现,60min达到高峰,而GCV对ERK1／2无明显的抑制作用。结论:中药金叶败毒制剂可通过调节MAPK／ERK通路而抑制HCMV基因的表达和复制从而发挥其部分抗病毒作用。Objective： To explore the mechanism of Jinyebaidu in treating human cytomegalovirus （HCMV） infection bstudying its depressant effect on mitogen-activated protein kinase （MAPK） /extracellular signal-regulated kinase including p44mapk （ERK1）and p42mapk （ERK2）. Methods： Expression of ER.K1/2 was evaluated by western blot analysis and the development of cytopathic effect （CPE） was also observed using HCMV infected human embryonic fibroblast as a model. Results： Jinyebaidu and PD98059 could inhibit HCMV proliferation in human embryonic lung （HEL）; furthernaore, inhibition of activation of ERK by Jinyebaidu occurred early during HCMV infection, ganciclovir （GCV） did not inhibit activation of ER.K. Conclusions： Jinyebaidu could inhibit the gene expression and duplication of HCMV possibly in ERK-MAPK dependent manner just as PD98059.

关 键 词：巨细胞病毒 丝裂素活化蛋白激酶 PD 98059 中药金叶败毒制剂 

分 类 号：R285[医药卫生—中药学]