【摘要】 目的:研究四硫化四砷(As4S4)对人胃癌细胞SGC7901增殖的抑制作用及其作用机制。方法:体外培养SGC7901,取对数生长期的细胞分为空白对照组(不加药物)和20、40、60、80μmol/LAs4S4处理组,分别作用24、48、72 h。采用MTT法检测细胞增殖的抑制率,透射电镜观察细胞的形态,流式细胞仪分析细胞的周期分布,逆转录-聚合酶链式反应法和蛋白质印迹法检测作用48 h后细胞中凋亡相关基因Bcl-2、Bax mRNA和蛋白的表达。结果:与空白对照组比较,20(作用48、72 h)、40、60、80μmol/LAs4S4处理组细胞增殖的抑制率明显升高(P<0.01),与浓度和时间呈正相关;从40μmol/L As4S4处理组细胞开始出现凋亡,60μmol/L As4S4处理组细胞开始出现大量凋亡,细胞周期阻滞于S期;与空白对照组比较,As4S4处理组细胞中Bcl-2 mRNA和蛋白表达随As4S4浓度的增加而减弱,Bax mRNA和蛋白表达随As4S4浓度的增加而增强。结论:As4S4具有抑制SGC7901细胞增殖的作用,其机制可能与诱导细胞凋亡、下调Bcl-2表达、上调Bax表达有关。更多还原

【Abstract】 OBJECTIVE:To study the inhibitory effect of As4 S4 on the proliferation of human gastric cancer SGC7901 cells and its mechanism. METHODS:SGC7901 cells were treated in vitro,and those at logarithmic growth phase were divided into blank control group(untreated)and 20,40,60 and 80 μmol/L As4 S4 treatment group(treated for 24,48 and 72 h). MTT method was used to examine the inhibitory rate of As4 S4 on SGC7901 cells. TEM was used to observe morphologic change of cells,and FCM assay was performed to measure cell cycle. RT-PCR method and Western blot were used to detect the mRNA and protein expression of Bcl-2 and Bax. RESULTS:Compared with blank control group,the inhibitory rates to cell proliferation were increased significantly in 20(treated for 48,72 h),40,60 and 80 μmol/L As4 S4 treatment group(P<0.01),positively associating with concentration and time. The apoptosis of SGC7901 cells appeared in 40 μmol/L As4 S4 treatment group;and a great many of apoptotic cells appeared in 60 μmol/L As4 S4 treatment group and the cell cycle was arrested in S phase. Compared with blank control group, mRNA and protein expression of Bcl-2 in As4 S4 treatment group decreased as the increase of As4 S4 concentration;the mRNA and protein expression of Bax increased as the increase of As4 S4 concentration. CONCLUSIONS:As4 S4 is effective to inhibit the proliferation of SGC7901 cells,and the mechanism might be relevant to induction of cell apoptosis,down-regulation of Bcl-2 expression and up-regulation of Bax expression.更多还原