雷公藤甲素对人肝细胞L-02钙离子及P38MAPK磷酸化的影响  

Effects of triptolide on Ca^(2+) and MAPK in human liver cell line L-02 cells

作　　者：姚金成[1] 刘颖[1] 胡领[2] 张陆勇[3] 饶健[1] 曾令贵[1] 江振洲[3] 何玲[3] 

机构地区：[1]湖南省药品审评认证与不良反应监测中心,湖南长沙410013 [2]中南大学湘雅二医院,湖南长沙410011 [3]中国药科大学国家新药筛选中心,江苏南京210009

出　　处：《中国医院药学杂志》2013年第10期760-763,共4页Chinese Journal of Hospital Pharmacy

基　　金：财政部行业科研专项资助课题(编号:200707008);湖南省科技厅科技计划项目(编号:2009FJ3027)

摘　　要：目的:研究雷公藤甲素对正常人肝细胞株L-02细胞凋亡诱导的作用及对细胞内钙离子及p38MAPK磷酸化的影响。方法:体外培养L-02细胞,Fluo-3AM标记与PI法观察雷公藤甲素对细胞的损伤作用,并测定雷公藤甲素作用下L-02细胞内钙离子浓度及Phospho-p38与Total-p38的含量。结果:雷公藤甲素体外诱导L-02细胞损伤,随着孵育时间的延长,细胞内钙离子浓度升高,至9h时达峰值(P<0.01),12h时有所下降(P<0.05);同时,雷公藤甲素促进细胞中P38MAPK的磷酸化(P<0.01),但对Total-p38无影响。结论:细胞内钙离子的释放及p38MAPK的磷酸化可能参与了雷公藤甲素引起的L-02细胞毒性。OBJECTIVE To investigate the apoptosis-inducing effects of triptolide on human liver cells L-02 in vitro and the changes of concentration of Ca2＋ and the phosphorylation of p38MAPK.METHODS The lesion effects of triptolide were investigated by marking the cells with Fluo-3AM or stained with PI.The concentration of Ca2＋ and the phosphorylation of p38MAPK were detected.RESULTS Triptolide caused cell injury in vitro.Ca2＋ concentration was markedly promoted and it accumulated to max value when cultured at 9 h（P0.01）,while it decreased at 12 h（P0.05）.Triptolide significantly promoted the phosphorylation of p38MAPK,but there was no significant change in Total-p38.CONCLUSION Triptolide induced injury of L-02 cells,which was associated with Ca2＋ generation and the phosphorylation of p38MAPK.

关 键 词：雷公藤甲素 人肝细胞株L-02 凋亡 钙离子 MAPK 

分 类 号：R963[医药卫生—微生物与生化药学]