蟾毒灵诱导人肝癌细胞HepG2凋亡的作用及机制  

Effect of apoptosis induced by bufalin on hunman hepatocarcinoma cell line HepG2 in vitro

作　　者：张宁[1,2] 汪晨[1] 顾伟[1] 凌昌全[1] 

机构地区：[1]中国人民解放军第二军医大学附属长海医院中医科,上海200433 [2]中国人民解放军第302医院

出　　处：《中西医结合肝病杂志》2009年第6期343-345,I0007,共4页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases

基　　金：国家自然科学基金青年科学基金(No.30200364)

摘　　要：目的:探讨蟾毒灵对人肝癌细胞系HepG2的凋亡诱导作用及其相关机制。方法:采用Annexin V-FITC/PI标记方法,观察蟾毒灵对HepG2细胞的凋亡诱导效应;用Western blot方法检测蟾毒灵对细胞凋亡相关蛋白及信号通路的影响。结果:①蟾毒灵能够诱导HepG2细胞凋亡。②蟾毒灵能够上调bax蛋白并下调bcl-2蛋白的表达水平。③蟾毒灵作用于HepG2细胞后,能够抑制PKB/Akt蛋白的磷酸化但促进JNK1/2的磷酸化。结论:蟾毒灵能够诱导HepG2细胞凋亡,该作用可能与其改变凋亡相关蛋白的表达水平和增殖相关信号通路的活化状态有关。Objective： To study the effect of bufalin on inducing apoptosis of hepatocellular carcinoma cell line HepG2 and the involved mechanism. Methods： Apoptosis of HepG2 cell labelling with Annexin V-FITC/PI was observed by flow cytometry ; Western blot was performed to detect the expressioff of signaling molecules related to apoptosis. Results： （1）Bufalin could induce apoptosis of HepG2 cell in vitro. （2）Bufalin could upregulate the expression of bax protein and downregulate the expression of bcl- 2 protein. （3）The phosphorylation of PKB/Akt was inhibited but JNK1/2 phosphorylation was promoted after bufalin incubation. Conclusion： Bufalin can trigger apoptosis of HepG2 cell by regulating the critical signaling pathways and molecules related to cell growth.

关 键 词：蟾毒灵/药效学 肝癌 信号通路 细胞凋亡 

分 类 号：R735.7[医药卫生—肿瘤]