论文部分内容阅读
目的 探讨环氧合酶 - 2 (COX -2 )特异抑制剂SC2 36诱导胃癌细胞凋亡的机制。方法SC2 36处理AGS细胞后 ,吖嘧橙染色观察细胞凋亡 ,免疫印迹法检测凋亡相关蛋白、细胞色素C水平。caspase- 3的激活通过免疫印迹法检测其活性片段、其底物多聚 (ADP 核糖 )聚合酶 (PARP)的裂解和比色法检测其催化活性来确定。结果 SC2 36处理AGS细胞可明显提高前凋亡蛋白Bak的水平 ,促使细胞色素C从线粒体进入胞浆 ,并激活caspase 3。caspase 3的特异抑制剂z DEVD fmk可以抑制SC2 36诱导的凋亡 ,细胞凋亡率由 (33.4± 3.2 ) %下降到 (16 .1± 1.5 ) %。结论 SC2 36至少部分通过上调Bak、促进细胞色素C的释放以及激活caspase 3的途径诱导胃癌细胞凋亡。
Objective To investigate the mechanism of cyclooxygenase-2 (COX-2) specific inhibitor SC2 36 in apoptosis of gastric cancer cells. Methods AG2 cells were treated with SC2 36, and acinitrin staining was used to observe apoptosis. Western blotting was used to detect apoptosis related protein and cytochrome C levels. The activation of caspase-3 was detected by Western blotting and its catalytic activity was determined by cleavage of its substrate poly (ADP ribose) polymerase (PARP) and its colorimetric assay. Results Treatment of AGS cells with SC2 36 significantly increased the level of pro-apoptotic protein Bak, promoted the entry of cytochrome C from the mitochondria into the cytoplasm, and activated caspase 3. z DEVD fmk, a specific inhibitor of caspase 3, could inhibit the apoptosis induced by SC2 36, and the apoptotic rate decreased from (33.4 ± 3.2)% to (16.1 ± 1.5)%. Conclusion SC2 36 induces apoptosis in gastric cancer cells at least partly by up-regulating Bak, promoting the release of cytochrome C and activating caspase 3.