中文摘要：

目的：探讨氯通道阻断剂5-硝基-2-（3-苯丙胺）苯甲酸（NPPB）对人脑胶质瘤SHG-44细胞凋亡的诱导作用,并阐明其可能的机制。方法：体外培养脑胶质瘤SHG-44细胞,分为对照组及50、100和200μmol·L^-1 NPPB组。采用MTT法检测细胞活力,采用流式细胞术检测细胞凋亡率,采用免疫组织化学法和蛋白免疫印记法分别检测SHG-44细胞中凋亡蛋白的表达水平。结果：MTT检测,与对照组比较,作用24和48h,100和200μmol·L^-1 NPPB组SHG-44细胞活力明显降低（P〈0.01）。流式细胞术检测,100和200μmol·L^-1 NPPB组细胞凋亡率分别为24.64%和41.85%,高于对照组（4.17%）（P〈0.01）。免疫组织化学和蛋白免疫印记法检测,100μmol·L^-1 NPPB组SHG-44细胞中caspase-3和Bax蛋白表达水平升高（P〈0.05或P〈0.01）,Bcl-2蛋白表达水平降低（P〈0.05）。结论：NPPB可以通过下调Bcl-2的表达、上调Bax的表达,使caspase-3活化,进而引起SHG-44细胞凋亡。

英文摘要：

Objective：To investigate the induction effect of NPPB,a chloride channel blocker,on the apoptosis of human glioma SHG-44 cells,and to explore its mechanism.Methods：The SHG-44 cells were cultured in vitro and divided into control group and NPPB groups（50,100,200μmol·L^-1）.The cell viability was detected by MTT assay.The apoptotic rates were detected by flow cytometry.The expression levels of Bax,Bcl-2and caspase-3were detected by immunohistochemical analysis and Western blotting method.Results：Compared with control group,the cell viabilities of SHG-44 cells in 100 and 200μmol·L^-1 NPPB groups after treated for 24and48 hwere decreased significantly（P〈0.01）.The results of flow cytometry showed that the apoptotic rates of SHG-44 cells in 100 and 200μmol·L^-1 NPPB groups were 24.64% and 41.85%,and they were higher than that in control group（4.17%）（P〈0.01）.The immunohistochemical analysis and Western blotting results showed that the expression levels of caspase-3and Bax proteins in SHG-44 cells in 100μmol·L^-1 NPPB group were increased（P〈0.05 or P〈0.01）,and the expression level of Bcl-2 protein was decreased（P〈0.05）.Conclusion：NPPB could induce the apoptosis of human glioma SHG-44 cells by the down-regulation of the expression of Bcl-2and the up-regulation of the expression of Bax,and the activation of caspase-3.