Brivanib对HepG2细胞的抑制作用及机制  

Inhibitory effect and mechanism of Brivanib on HepG2 cells

作　　者：韩兴华[1] 王章桂 

机构地区：[1]安徽医科大学附属安徽省立医院,安徽合肥230001 [2]安徽省第二人民医院,安徽省职业病医院,安徽合肥230001

出　　处：《现代肿瘤医学》2017年第3期355-357,共3页Journal of Modern Oncology

基　　金：安徽省科技攻关项目(编号:1401042007)

摘　　要：目的:探讨Brivanib对人Hep G2肝癌细胞的增殖抑制作用及其机制。方法:MTS法检测Brivanib对Hep G2细胞的增殖抑制作用,流式细胞仪检测不同浓度Brivanib处理后Hep G2细胞的凋亡率,Western blot检测凋亡相关蛋白Bcl-2、Bax的表达情况,免疫荧光观察Brivanib处理后Hep G2细胞内源性LC3表达情况,Western blot检测自噬关键蛋白LC-I向LC-II的转换及p62的表达。结果:与空白对照组相比,Brivanib对Hep G2肝癌细胞的增殖抑制率随剂量增加和时间延长而增加,呈剂量和时间依赖性。不同浓度Brivanib作用72h后Hep G2细胞的凋亡率分别为(13.06±4.06)%、(20.89±1.83)%、(44.29±2.56)%,其诱导凋亡与下调Bax、上调Bcl-2表达相关。2.5μmol/L Brivanib处理Hep G2细胞48h后内源性LC3表达增加。Western blot分析表明,LC3-I向LC3-II转换增加,p62表达降低。结论:Brivanib抑制Hep G2人肝癌细胞增殖,诱导凋亡和自噬活化。Objective：To explore the inhibitory effect and mechanism of Brivanib on human hepatocellular carci-noma HepG2 cells. Methods：The anti - proliferative effect of Brivanib on HepG2 cells were assessed by MTS. HepG2 cell apoptosis rate was determined by flow cytometry（FCM）analysis after various concentration Brivanib treatment. The expressions of Bcl - 2 and Bax were detected by Western blot. The expression of LC3 were examined by immuno-fluorescence and Western blot. Results：The anti - proliferative rates were increased in dose - dependant and time -dependant manners. After incubated with different doses of Brivanib,the inhibitory rates of HepG2 cells were（13. 06 ± 4. 06）% ,（20. 89 ± 1. 83）% and（44. 29 ± 2. 56）% ,respectively. The apoptosis rates were（13. 06 ± 4. 06）% , （20. 89 ± 1. 83）% and（44. 29 ± 2. 56）% ,respectively. Which were correlated with the decreasing of Bax and in-creasing of Bcl - 2. Furthermore,the expression of LC3 was increased by 2. 5μmol/ L Brivanib treatment,and p62 de-creased. Conclusion：Brivanib inhibits the proliferation of HepG2 cells,induces apoptosis and activates autophagy.

关 键 词：肝细胞癌 Brivanib 凋亡 自噬 

分 类 号：R735.7[医药卫生—肿瘤]