中文摘要：

目的研究P13K／Akt通路在TRAIL诱导凋亡中的作用，以及奥沙利铂对TRAIL诱导胃癌BGC823细胞凋亡的影响。方法MTT法检测细胞存活率。流式细胞术检测细胞凋亡。Westernblot法检测Akt，p-Akt蛋白表达。结果100ng／mL的TRAIL作用BGC823细胞16h，只引起轻度的细胞凋亡。TRAIL可活化P13K／Akt通路，P13K抑制剂LY294002（25μmol／L）预处理细胞1h后再予TRAIL作用16h，细胞凋亡比率明显升高（12．7％±3．1％vs3．5％±1．1％，P〈0．05）。38μg/mL奥沙利铂可抑制P13K／Akt通路的活化，进而增强细胞对TRAIL的敏感性，细胞凋亡率提高到35．5％±4．5％，P〈0．05。结论奥沙利铂通过抑制TRAIL诱导的P13K／Akt活化，增强胃癌BGC823细胞对TRAIL的敏感性。

英文摘要：

Objective To investigate the role of phosphoinositide 3-kinases （PI3K）/Akt signaling pathway in TRAIL-induced cell apoptosis, and the effect of oxaliplatin on TRAIL-induced apoptosis in gastric cancer BGC823 cells. Methods Cell proliferation was roeasured using MTT assay. Cell apoptosis was determined by flow eytoroetry. The expression of Akt and phospbor-Akt were determined by Western blotting. Results 100 ng/mL TRAIL caused little cell apoptosis in BGC823 cells. TRAIL activated P13K/Akt pathway. Pretreated with PI3K in- hibitor LY294002 （25 μmol/L）for 1 h followed by exposure to TRAIL for 16 h,the cell apoptosis was obviously higher （12.7%±3,1% vs 3.5%±1.1% ,P 〈 0.05） than that without the treatment of LY294002. Treatment with 38 μg/mL oxaliplatin blocked the activation of P13K/ Akt signaling, and enhanced the sensitivity of cells to TRAIl,, the rate of cell apoptosis increased to 35.5%±4.5% （P 〈 0.05 ）. Conclusion Oxaliplatin enhanced the sensitivity of gastric cancer BGC823 cells to TRAIL by inhibiting TRAIL-induced the activation of PI3K/Akt pathway.