亚硒酸钠抑制人胃癌BGC823细胞的作用及其机制探讨

THE ANTITUMOR EFFECT AND MECHANISM OF SODIUM SELENITE ON HUMAN GASTRIC CANCER CELL LINES BGC823 IN VITRO

目的观察亚硒酸钠对体外培养的人胃癌BGC823细胞增殖的抑制作用及其作用机制。方法用不同浓度(0、4.0、8.0、10.0μmol/L)的亚硒酸钠处理BGC823细胞24h后,采用四甲基偶氮噻唑蓝比色法(MTT法)检测亚硒酸钠对细胞的增殖抑制作用,流式细胞仪PI染色检测细胞周期,AnnexinV/PI双染法定量检测BGC823细胞凋亡率,FAS蛋白染色流式细胞仪定量检测各实验组细胞间FAS蛋白表达,荧光显微镜观察DAPI染色细胞形态。结果亚硒酸钠可明显抑制BGC823胃癌细胞的增殖,呈剂量依赖性;亚硒酸钠可阻滞细胞于S期和增加BGC823胃癌细胞凋亡率并随剂量增大作用增强;DAPI染色观察到亚硒酸钠给药组出现细胞核浓缩、边缘化以及凋亡小体等细胞凋亡的形态特征;亚硒酸钠可呈剂量依赖地增强FAS蛋白表达。结论亚硒酸钠可显著抑制人BGC823胃癌细胞的增殖,使细胞阻滞于S期,并可诱导细胞凋亡,其机制可能与上调FAS蛋白有关。

Objective To investigate the inhibitory effect of sodium selenite on human gastric cancer cell lines BGC823 and its possible mechanism. Methods The inhibitory effects of sodium selenite with different concentrations（0, 4.0, 8.0, 10.0μmol/L） on BGC823 cells were detected by MTT assay. The cell cycle distribution was measured by flow cytometry （FCM）. The apoptosis was examined by AnnexinV-FITC/PI staining. The apoptosis morphology was observed by fluorescence microscope after DAPI staining. FCM was used to quantitate the expression of FAS. Results MTT assay showed that sodium selenite inhibited the growth of BGC823 gastric cancer cells dose-dependently. Sodium selenite blocked BGC823 cells in S phase and increased the apoptosis rates of BGC823 cells dose-dependently. The typical apoptotic morphological changes including cell nucleus shrinkage, chromatin condensation and apoptotic bodies were observed when treated with different doses of sodium selenite. FCM showed that sodium selenite increased expressions of FAS dose- dependently. Conclusion Sodium selenite could inhibit human BGC823 gastric cancer cells proliferation and block cell cycle in S phase and induce apoptosis.The upregulation of FAS protein might be one of the mechanisms.