三氧化二砷诱导肝癌细胞系HepG-2自噬及其机制研究  

Study of HepG-2 cells’ autophagy induced by arsenic trioxide and its mechanism

作　　者：朱传升[1] 侯明[2] 王金慎[1] 王焱[1] 徐文伟[1] 董琳[1] 

机构地区：[1]山东省千佛山医院血液科,山东济南250014 [2]山东大学齐鲁医院血液科,山东济南250012

出　　处：《中国现代普通外科进展》2007年第4期302-305,共4页Chinese Journal of Current Advances in General Surgery

摘　　要：目的:测定不同浓度三氧化二砷(As2O3)诱导前后HepG-2细胞自噬水平改变,并初步探讨机制。方法:常规细胞培养,按As2O3不同浓度分组;采用MDC染色,荧光显微镜观察自噬囊泡,流式细胞术检测其荧光强度;RT-PCR检测Bcl-2基因转录,免疫组织化学检测细胞Bcl-2蛋白阳性百分率,并分析同自噬的关系。结果:经不同浓度As2O3作用后,HepG-2细胞生长明显受到抑制;荧光显微镜可观察到自噬囊泡的出现;Bcl-2基因表达降低;经相关性分析,HL-60细胞自噬水平与Bcl-2基因表达呈负相关。结论:As2O3可诱导HepG-2细胞自噬,v诱导HepG-2细胞自噬的机制可能与下调Bcl-2基因表达有关,自噬和凋亡存在交叉。Objective： To assess the level of autophagy and its mechanism in HepG-2 cells after induction with arsenic trioxide. Methods： The autophagy was analyzed using fluorescent microscope and flow cytometry by monodansylcadaverin（MDC） staining. RT-PCR was used to examine the Bcl-2 mRNA expression. APAAP was used to detect Bcl-2 protein positive percentage and its correlation with autophagy level was analyzed. Results： HL-60 cells＇ growth was obviously inhibited after induction with different density arsenic trioxide; autophagy vesica was observed using fluorescent microscope; Bcl-2 gene expression was inhibited; cells autophagy level was negative correlated with Bcl-2 gene expression Conclusion： Arsenic trioxide may induce HpG-2 cells to autophagia and its main mechanism was to down-regulate bcl-2 gene expression.

关 键 词：自噬 基因 BCL-2 三氧化二砷 肝肿瘤 细胞 培养的 

分 类 号：R735.7[医药卫生—肿瘤]