CAJ | 학술논문

目的观察人参皂甙肠道代谢物Compound K (CK)对人胃癌细胞BGC823细胞增殖、凋亡的影响.方法实验分组:对照组(PBS溶液),实验组(浓度分别为2.5、5、7.5、10 μmol/L).噻唑蓝(MTT)比色法分别检测CK作用于细胞后其活力及生长抑制率;流式细胞术检测CK作用后细胞周期时相、凋亡率;免疫印迹法(Western blot)检测凋亡相关蛋白的表达.结果 5μmol/L CK作用细胞48 h时,细胞生长周期阻滞于G2/M期,细胞凋亡率为(21.17±3.16)％;Western blot检测显示Bcl-2,Bid蛋白表达随着药物浓度的增加而减少,Fas和Fas-L蛋白表达量却没有明显变化.结论 CK是通过线粒体介导的凋亡通路途径来诱导人胃癌细胞发生凋亡的.
목적 관찰인삼조대장도대사물Compound K (CK)대인위암세포BGC823세포증식、조망적영향.방법 실험분조:대조조(PBS용액),실험조(농도분별위2.5、5、7.5、10 μmol/L).새서람(MTT)비색법분별검측CK작용우세포후기활력급생장억제솔;류식세포술검측CK작용후세포주기시상、조망솔;면역인적법(Western blot)검측조망상관단백적표체.결과 5μmol/L CK작용세포48 h시,세포생장주기조체우G2/M기,세포조망솔위(21.17±3.16)％;Western blot검측현시Bcl-2,Bid단백표체수착약물농도적증가이감소,Fas화Fas-L단백표체량각몰유명현변화.결론 CK시통과선립체개도적조망통로도경래유도인위암세포발생조망적.
Objective To investigate the effect of CK on proliferation,apoptosis of BGC823 cells.Methods BGC823 cells were treated with CK at different concentrations,cell viability was assayed using MTT methods.Cell cycle,apoptosis rate were assayed by flow cytometry.The expression of apoptosis-related protein were detected by Western blotting.Results After BGC823 cells were treated with 5 μmol/L CK for 48 h,the growth cycle was arrested on G2/M phase,the apoptosis rate was (21.17 ± 3.16)％.The expressions of Bcl-2,Bid protein was down-regulated after CK treatment,while the Fas and Fas-L protein were not significantly changed.Conclusions CK inhibits proliferation of BGC823 cells,and induces apoptosis via mitochondrion-mediated pathway.