亚砷酸钠对人胃癌细胞株BGC-823的作用机制  

Antitumor Mechanism of Sodium Arsenic on Human Gastric Carcinoma Cell Line BGC-823 in Vitro

作　　者：赵文韬[1] 王严庆[1] 汤为学[2] 

机构地区：[1]重庆医科大学附属第一医院普外科,400016 [2]重庆医科大学病理生理教研室

出　　处：《肿瘤防治研究》2006年第5期337-339,F0003,共4页Cancer Research on Prevention and Treatment

摘　　要：目的探讨亚砷酸钠对人胃癌细胞株BGC-823的作用机制。方法采用MTT法、光镜、电镜、流式细胞仪检测和免疫细胞化学法研究亚砷酸钠对BGC-823细胞生物学行为的影响。结果不同浓度的亚砷酸钠均可有效抑制BGC-823细胞生长,且具有浓度和时间依赖性,其中效浓度为4.86μmol/L。流式细胞仪检测发现亚砷酸钠作用不同时间后,细胞均出现G2/M期阻滞。形态学观察显示亚砷酸钠作用72h后,细胞出现典型的凋亡和坏死形态学改变。免疫细胞化学法发现亚砷酸钠能显著上调细胞Caspase-3蛋白的表达。结论亚砷酸钠对BGC-823细胞的生长有明显的抑制作用,并可诱导细胞周期阻滞及细胞凋亡和坏死,其机制可能与其抑制ROS的清除,上调Caspase-3蛋白的表达有关。Objective To investigate the antitumor mechanism of sodium arsenic on human gastric carcinoma cell line BGC-823 in vitro. Methods MTT assay, light microscopy,electron microscopy,flow cytometry, and imrnunocytochemical staining were used to detect the effect of sodium arsenic on biologic behavior of BGC-823 cells, Results Sodium arsenic inhibited the growth of BGC-823 cells in a time and concentration dependent fashion, its 50% inhibitory concentration（IC50 ） was 4. 86μmol/L. BGC-823 cells were arrested significantly in G2/M phase when treated with sodium arsenic. BGC-823 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenic. Sodium arsenic up-regulated Caspase-3 protein expression in BGC-823 cells, Conclusion Sodium arsenite could obviously inhibit the proliferation of BGC-823 cells： induce cell cycle arrest and apoptosis and necrosis of the cells, Its mechanism is possibly associated with inhibition of elimination of ROS, and the up-regulated expression of Caspase-3 protein.

关 键 词：亚砷酸钠 胃肿瘤 凋亡 CASPASE-3 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R735.205.3[医药卫生—基础医学]