特异性环氧合酶-2抑制剂SC236诱导胃癌细胞株凋亡的实验研究

目的:探讨环氧合酶-2(COX-2)特异性抑制剂SC236诱导胃癌细胞株SGC7901凋亡的机制. 方法: SC236对人胃癌来源的SGC7901细胞进行凋亡诱导.以吖啶橙染色后荧光显微镜下观察凋亡细胞形态并计算凋亡指数.Western blot法检测凋亡调节蛋白Bcl-2、Bak、Bax与CED-9的表达情况.流式细胞仪检测细胞凋亡率.结果: SGC7901细胞经SC236作用后,细胞中凋亡促进因子Bak的表达水平明显增高、凋亡抑制因子Bcl-2的表达水平显著下降、而凋亡促进因子Bax和凋亡抑制因子CED-9表达水平无明显变化.细胞凋亡指数或凋亡率则随SC236浓度的增加和作用的时间延长而升高.结论: COX-2特异抑制剂SC236可通过上调凋亡促进因子Bak表达和下调凋亡抑制因子Bcl-2表达而诱导胃癌细胞株SGC7901的凋亡.

Induction of apoptosis of gastric cancer cells by a specific COX-2 inhibitor SC236

Objective:To investigate the mechanism of apoptosis inducing effect of specific COX-2 inhibitor SC236 in gastric cancer cell line SGC7901. Methods: The expression level of apoptosis-regulating proteins Bcl-2,Bak,Bax and CED-9 was analyzed by Western blot method.Cell apoptosis index was measured by fluorescence microscopy as well as by flow cytometry. Results: Treatment of SGC7901 gastric cancer cells with SC236 caused a significant elevation of the expression of the apoptosis-promoting proteins Bak and Bax,but a significant reduction of the expression of the apoptosis-inhibiting protein Bcl-2 and CED-9 were observed.Cell apoptosis index or rate increased with the increment of SC236 concentration and the time of action. Conclusion: Specific COX-2 inhibitor SC236 could induce apoptosis in gastric cancer cell line SGC7901 through the up-regulation of the apoptosis-promoting proteins Bak and Bax,and the down-regulation of the apoptosis-inhibiting protein Bcl-2 and CED-9.