TRAIL联合紫杉醇诱导胃腺癌SGC-7901细胞凋亡作用研究

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(Westernblot)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);0.3μmol/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。

Experimental study on apoptosis of SGC-7901 cell induced by TRAIL combined with paclitaxel

Objective:The synergetic role of apoptosis in SGC-7901 cells by the combination of TRAIL and paclitaxel was investigate,to explore the potential mechanism of synergistic antitumor activity.Methods:SGC-7901 cells were treated with TRAIL or paclitaxel or TRAIL combined with paclitaxel for 48 h.The apoptotic rates and mitochondrial membrane potential were examined with flow cytometry(FCM).Proliferation of SGC-7901 cells was detected by MTT assay and expression of DR4/DR5 protein was detected by Western blot after treated with TRAIL combined with paclitaxel.Results:The inhibition rate of SGC-7901 cell increased obviously by combining TRAIL and paclitaxel,comparing with administration of TRAIL or paclitaxel alone,and the difference was statistically significant(P<0.01).The apoptosis rate of SGC-7901 cell increased obviously by combining TRAIL and paclitaxel(P<0.01).Expression of death receptor(DR4) was increased obviously(P<0.01) when SGC-7901 cells was treated with paclitaxel for 48 hours,but the death receptor(DR5) was not change obviously(P>0.05).Conclusion:Paclitaxel had synergetic role in the apoptosis effect induced by TRAIL in SGC-7901 cells.Up-regulating DR4 might be one of the reasons for synergetic antitumor activity.