CAJ | 학술논문

目的探讨β-二酮钴的配合物抑制人胶质瘤细胞U251增殖的机制.方法在经10、25 mg/L β-二酮钴的配合物处理48 h后人胶质瘤细胞U251中,通过光镜观察细胞形态变化,噻唑蓝(MTT)法分析细胞存活力变化;流式细胞术分析经10、25 mg/L β-二酮钴的配合物处理48 h后细胞周期的变化;最后通过Western blot分析10、25 mg/L β-二酮钴的配合物处理24h后周期相关蛋白的表达变化.结果 β-二酮钴的配合物抑制人胶质瘤细胞U251增殖并呈现剂量依赖性,半数抑制剂量(IC50)值为(25.30±4.22) mg/L,10％抑制剂量(IC10)值为(6.61±2.42) mg/L且抑制效果显著强于5-氟尿嘧啶(5-Fu);β-二酮钴的配合物诱导U251细胞发生S期阻滞,并呈现剂量依赖性;β-二酮钴的配合物诱导U251细胞周期蛋白(Cyclin)A和周期蛋白依赖性蛋白激酶2(CDK2)蛋白的表达下调,p21蛋白表达上调.结论 β-二酮钴的配合物抑制胶质瘤细胞U251是通过诱导细胞周期S期阻滞实现的.
목적 탐토β-이동고적배합물억제인효질류세포U251증식적궤제.방법 재경10、25 mg/L β-이동고적배합물처리48 h후인효질류세포U251중,통과광경관찰세포형태변화,새서람(MTT)법분석세포존활력변화;류식세포술분석경10、25 mg/L β-이동고적배합물처리48 h후세포주기적변화;최후통과Western blot분석10、25 mg/L β-이동고적배합물처리24h후주기상관단백적표체변화.결과 β-이동고적배합물억제인효질류세포U251증식병정현제량의뢰성,반수억제제량(IC50)치위(25.30±4.22) mg/L,10％억제제량(IC10)치위(6.61±2.42) mg/L차억제효과현저강우5-불뇨밀정(5-Fu);β-이동고적배합물유도U251세포발생S기조체,병정현제량의뢰성;β-이동고적배합물유도U251세포주기단백(Cyclin)A화주기단백의뢰성단백격매2(CDK2)단백적표체하조,p21단백표체상조.결론 β-이동고적배합물억제효질류세포U251시통과유도세포주기S기조체실현적.
Objective To investigate the mechanisms by which β diketone cobalt complexes inhibited human glioma U251 cells.Methods After treatment with β-diketone-cobalt complexes (10,25 mg/L) for 48 h,human glioma U251 cells were observed on the morphologies,analyzed with methyl thiazol tetrazolium (MTF) assay for cell proliferation,and assessed for the changes of cell cycle by flow cytometry.After treatment with β-diketone-cobalt complexes (10,25 mg/L) for 24 h,Western blotting was used to identify proteins involved in cell cycle.Results β-diketone-cobalt complexes suppressed human glioma U251 cells viability in a dose-dependent manner.50％ inhibitory dose (IC50) of β-diketone-cobalt complexes was (25.30 ± 4.22) mg/L,and 10％ inhibitory dose (IC10) was (6.61 ± 2.42) mg/L.β-diketone-cobalt complexes induced S arrest in U251 cells,increased the p21 and decreased cyclin A and cyclin-dependent kinase 2 (CDK2) expression.Conclusion β-diketone-cobalt complexes show an inhibitory effect against human glioma U251 cells by inducing the S arrest of cell cycle.