DEAB促进肝癌细胞凋亡及增强其对ADM敏感性的机制研究  

Research on the Mechanisms of the DEAB induced Apoptosis and chemotherapy sensitivity enhancement of ADM in hepatoma carcinoma cells

作　　者：张俊 薛新波[1] 申铭 郑建伟 肖朝文[2] Yu Yuan 

机构地区：[1]华中科技大学同济医学院附属同济医院胆胰外科,湖北武汉430030 [2]华中科技大学同济医学院附属武汉市中心医院肝胆胰外科,湖北武汉430014 [3]Dept. of Pancreatic Surgery,Tongji Hospital Affiliated to Tongji Medical College,Huazhong University of Science and Technology

出　　处：《泰山医学院学报》2017年第12期1328-1330,共3页Journal of Taishan Medical College

基　　金：华中科技大学同济医学院附属武汉中心医院博士科研基金(YB13B01);武汉市卫生计生委科研基金(WX14D07)

摘　　要：目的探讨ALDH抑制剂DEAB致肝癌细胞凋亡及增强其对ADM化疗敏感性的具体机制。方法通过DEAB干预肝癌细胞系HepG2和正常肝细胞系L02以及与经ADM处理的HepG2和L02细胞。通过流式细胞仪检测各组细胞中活性氧(ROS)的表达变化及Annexin-V和PI双染后细胞凋亡量的变化。通过Realtime PCR及western blot方法检测各组细胞中Bcl-2、Bax、ALDH1以及MDR1基因和蛋白的变化。结果 DEAB干预HepG2细胞后,致使其ROS表达增强、凋亡量增加,ALDH1基因和蛋白表达无明显变化,Bcl-2、MDR1基因和蛋白表达下调,Bax基因和蛋白表达上调。正常肝细胞系L02无以上变化。结论抑制ALDH可致肝癌细胞系HepG2凋亡,并增强其对ADM的化疗敏感性。而对正常肝细胞系L02无此作用。Objective: To investigate the mechanisms of the DEAB( ALDH inhibitor) induced apoptosis and chemotherapy sensitivity enhancement of ADM in hepatoma carcinoma cells. Methods: We interposed the Hep G2 cells、normal liver cell line L02 and Hep G2、L02 cells were treated by ADM with DEAB. Changes of expression of reactive oxygen species( ROS) and apoptosis were detected by flow cytometry in the each group. Changes in gene and protein level of ALDH1,Bcl-2 and of Bax and MDR1 were detected by Realtime PCR and western blot. Results: The function of ALDH were inhibited in Hep G2 cells,resulting in increased expression of ROS and apoptosis; expression of Bcl-2 and MDR-1 gene and protein were down regulation; expression of Bax gene and protein was up regulation; there were no such changes in the normal liver cell line L02. Conclusion: The apoptosis of Hep G2 cells was induced and the ADM sensitivity to chemotherapy was enhanced by the inhibition of ALDH,but there was no effect in the normal liver cell line L02.

关 键 词：DEAB ROS 线粒体凋亡 肝癌 化疗 ALDH 

分 类 号：R735.7[医药卫生—肿瘤]