β-二酮钴的配合物通过诱导S期阻滞抑制人胶质瘤细胞增殖

Effects of β-diketone - cobalt complexes on proliferation of human glioma U251 cells

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。方法彳F经10、25mg／L β-二酮钴的配合物处理48h后人胶质瘤细胞U251中，通过光镜观察细胞形态变化，噻唑监（MTT）法分析细胞存活力变化；流式细胞术分析经10、25mg／L β-二酮钴的配合物处理48h后细胞周期的变化；最后通过Westernblot分析10、25mg／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13-二酮钻的配合物抑制人胶质瘤细胞U251增殖并呈现剂量依赖性，半数抑制剂置（IC50）值为（25．30±4．22）mg／L，10％抑制剂量（IC10值为（6．61±2．42）mg／L且抑制效果渺簧强于5-氟尿嘧啶（5-Fu）；β-二酮钴的配合物诱导U25l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-二酮钻的配合物抑制胶质瘤细胞U251是通过诱导细胞川期S期阻滞实现的。

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 th- iazol tetrazolium （MTT） assay for cell proliferation, and assessed for the changes of cell cycle by flow cy- lometry. 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-dike- tone - 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 deereased 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.