亚砷酸钠对人胃癌细胞株SGC-7901作用机制的研究

 目的 探讨亚砷酸钠对人胃癌细胞株SGC-7901生物学行为的影响及其作用机制。方法采用MTT法、光镜、电镜、流式细胞仪检测和免疫细胞化学方法研究亚砷酸钠对人胃癌细胞株SGC-7901生物学行为的影响。结果 不同浓度（2.50～40.00 μmol／L）的亚砷酸钠均能抑制SGC-7901细胞生长，且具有浓度和时间依赖性，其作用72 h的中效浓度为8.69 μmol／L。流式细胞仪检测发现亚砷酸钠作用48 h，72 h后， SGC-7901细胞出现G2／M期阻滞。形态学观察显示亚砷酸钠作用72 h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SGC-7901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。

The study of antitumor mechanism of sodium arsenite on gastric carcinoma cell line SGC-7901 in vitro

Objective To investigate the antitumor mechanism of sodium arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MTT assay, light microscopy, electron microscopy, flow cy－tometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic be－havior of SGC-7901 cells. Results Sodium arsenite (2.50 ～ 40.00 μmol/L) could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration(IC50) was 8.69 μmol/L after 72 hours' treatment. SGC-7901 cells were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 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.