CAJ | 학술논문

目的：研究Akt抑制剂MK-2206对U2OS细胞凋亡和自噬的影响。方法：采用MTT法检测MK-2206对U2OS细胞活力的影响，DNA片段末端标记试剂盒检测细胞凋亡的变化，免疫印迹法检测细胞内蛋白的表达，用LC3-II的表达量用来确定细胞的自噬水平。结果： MK-2206剂量依赖性地降低了U2OS细胞的活力；MK-2206能够促进caspase-9、caspase-3和PARP的活化切割而诱导U2OS细胞发生凋亡；MK-2206给药后可促进细胞内LC3-II的表达，氯喹阻断自噬后明显增强了MK-2206对U2OS细胞活力的抑制作用。结论： Akt 抑制剂MK-2206能够诱导U2OS细胞发生凋亡和自噬；抑制自噬可促进MK-2206对U2OS细胞的毒性。
목적：연구Akt억제제MK-2206대U2OS세포조망화자서적영향。방법：채용MTT법검측MK-2206대U2OS세포활력적영향，DNA편단말단표기시제합검측세포조망적변화，면역인적법검측세포내단백적표체，용LC3-II적표체량용래학정세포적자서수평。결과： MK-2206제량의뢰성지강저료U2OS세포적활력；MK-2206능구촉진caspase-9、caspase-3화PARP적활화절할이유도U2OS세포발생조망；MK-2206급약후가촉진세포내LC3-II적표체，록규조단자서후명현증강료MK-2206대U2OS세포활력적억제작용。결론： Akt 억제제MK-2206능구유도U2OS세포발생조망화자서；억제자서가촉진MK-2206대U2OS세포적독성。
AIM:To observe the effect of MK-2206, an inhibitor of Akt, on the cell apoptosis and autophagy of U2OS cells.METHODS:The cell viability was detected by MTT assay .The cell apoptosis was analyzed by TdT-media-ted dUTP nick end labeling assay .The expression of LC3-II was examined by Western blotting .RESULTS:MK-2206 in-hibited the cell viability in a dose-dependent manner .MK-2206 induced the cell apoptosis via activation of caspase-3, caspase-9 and PARP.MK-2206 treatment substantially induced the U 2OS cell autophagy by increasing in the levels of LC 3-II.Blockage of autophagy using chloroquine magnified MK-2206-induced cell death in U2OS cells.CONCLUSION:The Akt inhibitor MK-2206 induces cell apoptosis and autophagy .Blocking autophagy magnifies MK-2206-induced the inhibi-tion of the viability in U2OS cells.