TRAIL联合紫杉醇诱导胃腺癌SGC-7901细胞凋亡作用研究

摘要

Objective:The synergelic role of apoplosis in SGC-7901 cells by the combination of TRAIL and paclilaxel was in-vesligale,lo explore the polential mechanism of synergistic anlilumor activily. Methods:SGC-7901 cells were Irealed with TRAIL or pa-clilaxel or TRAIL combined with paclilaxel for 48 h. The apoptotic rales and milochondrial membrane potential were examined wilh flow cylomelry (FCM). Proliferation of SGC-7901 cells was delecled by MTT assay and expression of DR4/DR5 prolein was delecled by Weslern blot after Lreated with TRAIL combined wilh paclilaxel. Results:The inhibilion rale of SGC-7901 cell increased obviously by combining TRAIL and paclilaxel,comparing wilh adminislralion of TRAIL or paclilaxel alone,and the difference was slalislically significant P＜0. 01). The apoplosis rale of SGC-7901 cell increased obviously by combining TRAIL and paclilaxel( P＜0. 01). Expression of dealh receplor (DR4) was increased obviously(P＜0. 01) when SGC-7901 cells was Irealed wilh paclilaxel for 48 hours, but the death receplor ( DR5 ) was nol change obviously( P＞0. 05 ). Conclusion:Paclilaxel had synergelic role in ihe apoplosis effecl induced by TRAIL in SGC-7901 cells. Up-regulating DR4 might be one of the reasons for synergelic anlilumor aclivily.%目的:观察紫杉醇联合肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导人胃腺癌SGC-7901细胞凋亡的作用及其协同作用机制.方法:将TRAIL、紫杉醇及TRAIL联合紫杉醇诱导SGC-7901细胞48小时,用流式细胞仪(FCM)检测细胞凋亡率和线粒体跨膜电位的改变;用MTT法检测SGC-7901细胞增殖反应;用免疫印迹(Western blot)法检测TRAIL死亡受体DR4(TRAIL-R1)、DR5(TRAIL-R2)的表达变化.结果:TRAIL和/或紫杉醇对SGC-7901细胞增殖有抑制作用,两者联合用药组对细胞增殖的抑制率较单独用药明显增加(P<0.01);联合用药组细胞凋亡率较单独用药组明显增加(P<0.01);0.3 μmol/L紫杉醇作用48小时后,DR4表达明显升高(P<0.05),而DR5表达没有明显改变(P>0.05).结论:紫杉醇可协同TRAIL诱导SGC-7901细胞凋亡,DR4表达增加可能是其协同作用的机制.