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目的：明确Bax-Bcl-2异源二聚体与NSAIDs诱导胃癌细胞凋亡的关系。方法：以NSAIDs诱导胃癌细胞凋亡,并通过丫啶橙(AO)染色、共聚焦显微镜、流式细胞术、TUNEL法加以证实。应用Western blot方法检测Bax、Bcl-2蛋白的表达,应用免疫沉淀-蛋白印迹法检测Bax-Bcl-2异源二聚体水平的改变。结果：NSAIDs药物吲哚美辛(indomethacin,indo)800 mmol/L和阿司匹林(aspirin,Asp)8 mmol/L作用24 h后,AGS细胞发生显著的凋亡(Indo 800 mmol/L作用24 h凋亡率(9．34±1．99)%,48 h(38．97±3．36)%,Asp 8 mmol/L 48 h凋亡率(17．60±3．30)%。随着药物作用时间的延长,Bax-Bcl-2异源二聚体水平逐渐增高,在6～48 h内均呈现增强趋势,Bax蛋白表达的增强在6～24 h最为明显,Bcl-2蛋白未检测到。结论：NSAIDs可诱导胃癌细胞AGS凋亡；Bax-Bcl-2异源二聚体可能具有促进细胞凋亡的作用,也可能是NSAIDs调控肿瘤细胞凋亡的一个重要作用点。
Objective: To investigate the relationship between Bax-Bcl-2 heterodimers and NSAIDs-induced gastric cancer cell apoptosis. Methods: Apoptosis of gastric cancer cells was induced by NSAIDs and confirmed by AO staining, confocal microscopy, flow cytometry and TUNEL. Western blot was used to detect the expression of Bax and Bcl-2 protein. The level of Bax-Bcl-2 heterodimer was detected by immunoprecipitation-Western blot. Results: AGS cells were significantly apoptosis induced by 800 mmol / L indomethacin (indo) and 8 mmol / L aspirin (Asp) for 24 h (9.34 ± 1.99)%, 48 h (38.97 ± 3.36)%, Asp 8 mmol / L 48 h apoptosis rate (17.60 ± 3.30)%, The effect of Bax-Bcl-2 heterodimers increased gradually from 6 to 48 hours, and the increase of Bax protein was the most obvious at 6 to 24 hours, while the Bcl-2 protein was not detected .Conclusion: NSAIDs can induce AGS apoptosis in gastric cancer cells. Bax-Bcl-2 heterodimers may play an important role in promoting apoptosis and may also play an important role in regulating apoptosis of NSCIDs.