β-二酮钴的配合物对C6大鼠脑胶质瘤细胞抑制生长和诱导凋亡的作用

β-diketone-cobalt complexes induce growth inhibition and apoptosis in rat C6 glioma cells

目的研究β-二酮钴的配合物抑制c6大鼠脑胶质瘤细胞增殖的机制。方法经梯度浓度β-二酮钴的配合物处理的c6大鼠脑胶质瘤细胞进行MTT分析，了解其抗胶质瘤细胞的活性；药物处理后的胶质瘤细胞进行DAPI染色，通过荧光显微镜观察细胞形态变化；对药物处理后的细胞进行AnnexinV／PI染色，使用流式细胞术来分析细胞凋亡情况；使用Westernblot蛋白印迹法检测处理后的细胞Bcl-2和Bax蛋白表达情况。结果β-二酮钻的配合物抑制c6大鼠脑胶质瘤细胞的Ic，。值为（24．7±3．4）μg/ml，Ic。值为（4．4±1．5）μg/ml，并呈现剂量依赖性；处理后的胶质瘤细胞核内出现凋亡细胞典型特征。与对照相比，处理后细胞的凋亡细胞的百分数升高，呈剂量相关性；Bcl-2蛋白的表达下调，Bax蛋白表达上调，随着浓度升高，Bcl-2／Bax蛋白比显著下降。结论β-二酮钴的配合物在大于4．37μg/ml的低浓度条件下就具有抑制胶质瘤细胞的能力，且部分是通过诱导其发生凋亡发挥出来，而其诱导细胞凋亡是通过调节Bcl-2、Bax通路线粒体途径实现的。

Objective To investigate the mechanisms of β-diketone-cobah complexes inhibiting rat C6 glioma cell proliferation. Methods Rat C6 glioma cells were analyzed with MTF assay after treatment of β-diketone-cobalt complexes , for checking the roles of β-diketone-cobalt complexes in the cell growth inhibition; Apoptosis was assessed by DAPI staining and Annexin V/PI flow cytometry; Western blot was used to identify proteins involved in apoptosis induced by β-diketone-cobah complexes. Results β-diketone-cobah complexes suppressed rat C6 glioma cells viability in a dose-dependent manner; ICs0 of β-diketone-cobalt complexes was （ 24. 7 ± 3.4 ） μg/ml, and IC10 was （ 4. 4 ± 1.5 ） μg/ml; β-diketone-cohalt complexes induced apoptosis in rat C6 glioma cells and increased the ratio of Bax/Bcl- 2. Conclusions These resuhs suggest that β-diketone-cobah complexes show a good inhibitory effect against tumor, and the inhibiting effect against rat C6 glioma cells at least partially via apootosis.