摘要
目的探讨伊立替康和肿瘤坏死因子相关凋亡诱导配体(TRAIL)对胃癌SGC7901细胞凋亡的影响并初步探讨其作用机制。方法不同浓度的伊立替康和/或200μg·L-1TRAIL作用于人胃癌细胞SGC7901细胞,MTT检测细胞增殖能力;流式细胞术检测细胞凋亡;TRAIL和/或伊立替康作用SGC7901细胞后,Western-blot检测蛋白表达。结果 200μg·L-1的TRAIL对胃癌细胞的增殖抑制率为18.46%,TRAIL(200μg·L-1)联合伊立替康(28.67mg·L-1)引起明显的增殖抑制和细胞凋亡(P<0.05)。TRAIL(200μg·L-1)单药和伊立替康(28.67mg·L-1)单药都没有改变Bax、Caspase-8蛋白的表达,而两者联用增加了Bax、Caspase-8蛋白的表达。结论伊立替康通过增加Bax、Caspas-8蛋白表达来增强TRAIL诱导的胃癌SGC7901细胞凋亡。
OBJECTIVE To determine the effect and mechanism of tumor necrosis factor-related apoptosis-inducing ligand（TRAIL） combined with CPT-11 on apoptosis of human gastric cancer cell line SGC7901.METHODS Proliferation inhibitory rate of TRAIL and CPT-11 was examined by methyl thiazolyl tetrazolium（MTT） assay.Flow cytometry（FCM） was used to determine apoptosis after treatment of TRAIL and/or CPT-11.The expressions of Bax and Caspase-8 were detected by using Western-blot.RESULTS The proliferation inhibitory rate after 24 hour treatment of 200μg·L-1 was 18.46%.Combination therapy of TRAIL（200μg·L-1） and CPT-11（28.67mg·L-1） resulted in a synergistic cytoxic effect.Protein expression levels of Bax and Caspase-8 were enhanced in the group of TRAIL and CPT-11 combination compared with other groups（P0.05）.CONCLUSION Combination of TRAIL and CPT-11 induced apoptosis of gastric cancer cell line SGC7901,which may attribute to increasing the protein expression of Bax and Caspase-8.
出处
《海峡药学》
2012年第10期234-237,共4页
Strait Pharmaceutical Journal
