CAJ | 학술논문

　　目的：研究自噬对顺铂（cisplatin，DDP）诱导的胃癌SGC7901细胞凋亡的影响，并初步探讨其可能机制。方法：DDP和（或）氯喹处理胃癌SGC7901细胞，MTT法检测细胞增殖，流式细胞术检测细胞凋亡，MDC染色后荧光显微镜观察自噬囊泡，West-ern Blot检测自噬和凋亡相关蛋白。结果：5 mg/L的顺铂作用于胃癌SGC7901细胞24 h，细胞凋亡率为21.07%±2.12%，同时观测到自噬囊泡增多和LC3-Ⅱ蛋白表达升高；氯喹特异性抑制自噬活性后，提高了顺铂诱导的细胞凋亡率（30.16%±3.54%，P<0.05）；检测到凋亡相关蛋白Caspase-3和P53表达增加，Bcl-2蛋白表达下降。结论：自噬在顺铂诱导胃癌SGC7901细胞凋亡的过程中起保护作用，氯喹抑制自噬后，可能通过激活P53蛋白及灭活Bcl-2蛋白的表达来促进细胞凋亡，联合应用顺铂和氯喹有望成为胃癌治疗的新策略。
　　목적：연구자서대순박（cisplatin，DDP）유도적위암SGC7901세포조망적영향，병초보탐토기가능궤제。방법：DDP화（혹）록규처리위암SGC7901세포，MTT법검측세포증식，류식세포술검측세포조망，MDC염색후형광현미경관찰자서낭포，West-ern Blot검측자서화조망상관단백。결과：5 mg/L적순박작용우위암SGC7901세포24 h，세포조망솔위21.07%±2.12%，동시관측도자서낭포증다화LC3-Ⅱ단백표체승고；록규특이성억제자서활성후，제고료순박유도적세포조망솔（30.16%±3.54%，P<0.05）；검측도조망상관단백Caspase-3화P53표체증가，Bcl-2단백표체하강。결론：자서재순박유도위암SGC7901세포조망적과정중기보호작용，록규억제자서후，가능통과격활P53단백급멸활Bcl-2단백적표체래촉진세포조망，연합응용순박화록규유망성위위암치료적신책략。
Objective:To investigate the mechanism and effects of autophagy on cisplatin(DDP)-induced apoptosis in human gas-tric cancer cell line SGC7901. Methods:Cell proliferation was determined by an MTT assay after the SGC7901 cells were treated with DDP and/or chloroquine. Cell apoptosis was determined by flow cytometry. Autophagy and related protein expressions were detected by Western blot. Autophagy was quantitatively analyzed by fluorescence microscopy after monodansylcadaverine staining was per-formed. Results:The cells were treated with 5 mg/L of DDP for 24 h, the rate of cell apoptosis was (21.07 ± 2.12)%. Autophagy, char-acterized by an increase in the number of autophagic vesicles and LC3-II protein level, was observed in DDP-treated cells. After autoph-agy was inhibited by chloroquine, the rate of cell apoptosis was increased to (30.16 ± 3.54)%. In addition, caspase-3 and P53 protein levels were increased, but Bcl-2 protein was decreased. Conclusion:Autophagy protected human gastric cancer cell line SGC7901 from DDP-induced apoptosis. In addition, the inhibition of autophagy could promote apoptosis. The combined therapy of DDP and chlo-roquine may be a promising therapeutic strategy for gastric cancer.