【摘要】 目的探讨紫杉醇增强TRAIL诱导的胃癌BGC823细胞凋亡的机制。方法胃癌BGC823细胞传代培养后,取对数生长期细胞用于实验。采用MTT法测定细胞活力,流式细胞仪检测细胞凋亡,Western blot检测Akt、p-Akt蛋白表达。结果在胃癌BGC823细胞中,100 ng/ml的TRAIL可致少量的细胞凋亡,同时检测到Akt的磷酸化。紫杉醇作用胃癌BGC823细胞24 h,IC50剂量为8.97μg/ml。与单药TRAIL和紫杉醇相比,TRAIL(100 ng/ml)联合紫杉醇(8.97μg/ml,24 h的IC50剂量)对细胞的诱导凋亡作用明显增强(P<0.05)。免疫印迹结果显示,TRAIL(100 ng/ml)作用BGC823细胞24 h,活化了Akt蛋白,而8.97μg/ml的紫杉醇抑制了Akt的磷酸化。TRAIL(100 ng/ml)联合紫杉醇(8.97μg/ml)作用后,TRAIL引起的Akt磷酸化被抑制。结论紫杉醇通过抑制TRAIL引起的Akt磷酸化,从而增强了TRAIL诱导的胃癌BGC823细胞凋亡。更多还原

【Abstract】 Objective To observe the inhibition effect of paclitaxel on tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis in gastric cancer BGC823 cells.Methods Gastric cancer BGC823 cells were routinely subcultured,and the used cells were all from the logarithmic growth phase.Cell proliferation was measured using MTT assay.Cell apoptosis was determined by flow cytometry.The expressions of Akt and phosphor-Akt were determined by Western blotting.Results Treatment with 100 ng/mL TRAIL resulted in a little cell apoptosis in BGC823 cells.Meanwhile,the phosphorylation of Akt was detected.Treatment with paclitaxel for 24 hours,the IC50 dose was 8.97 μg/ml.Compared to treatment with TRAIL or paclitaxel alone,treatment with TRAIL(100 ng/ml) and paclitaxel(8.97 μg/ml,IC50 dose of 24 h) leaded to a dramatic increase in cell apoptosis(P<0.05).Western blotting showed that TRAIL(100 ng/ml) alone induced the activation of Akt for 24 hours in BGC823 cells.While 8.97 μg/ml paclitaxel significantly inhibited the phosphorylation of Akt.Treatment with TRAIL(100 ng/ml)and paclitaxel(8.97 μg/ml) also prevented the phosphorylation of Akt induced by TRAIL.Conclusion Paclitaxel enhance TRAIL-induced apoptosis in gastric cancer BGC823 cells by the inhibition of Akt phosphorylation induced by TRAIL.更多还原