CAJ | 학술논문

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Annexin V/PI染色,使用流式细胞术来分析细胞凋亡情况;使用Western blot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-二酮钴的配合物抑制C6大鼠脑胶质瘤细胞的IC50值为(24.7 ±3.4) μg/ml,IC10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4.37 μg/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.
목적 연구β-이동고적배합물억제C6대서뇌효질류세포증식적궤제.방법 경제도농도β-이동고적배합물처리적C6대서뇌효질류세포진행MTT분석,료해기항효질류세포적활성;약물처리후적효질류세포진행DAPI염색,통과형광현미경관찰세포형태변화;대약물처리후적세포진행Annexin V/PI염색,사용류식세포술래분석세포조망정황;사용Western blot단백인적법검측처리후적세포Bcl-2화Bax단백표체정황.결과 β-이동고적배합물억제C6대서뇌효질류세포적IC50치위(24.7 ±3.4) μg/ml,IC10치위(4.4±1.5) μg/ml,병정현제량의뢰성;처리후적효질류세포핵내출현조망세포전형특정.여대조상비,처리후세포적조망세포적백분수승고,정제량상관성;Bcl-2단백적표체하조,Bax단백표체상조,수착농도승고,Bcl-2/Bax단백비현저하강.결론 β-이동고적배합물재대우4.37 μg/ml적저농도조건하취구유억제효질류세포적능력,차부분시통과유도기발생조망발휘출래,이기유도세포조망시통과조절Bcl-2、Bax통로선립체도경실현적.
Objective To investigate the mechanisms of β-diketone-cobalt complexes inhibiting rat C6 glioma cell proliferation.Methods Rat C6 glioma cells were analyzed with MTT 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-cobalt complexes.Results β-diketone-cobalt complexes suppressed rat C6 glioma cells viability in a dose-dependent manner;IC50 of β-diketone-cobalt complexes was (24.7 ± 3.4) μg/ml,and IC10 was (4.4 ± 1.5) μg/ml; β-diketone-cobalt complexes induced apoptosis in rat C6 glioma cells and increased the ratio of Bax/Bcl-2.Conclusions These results suggest that β-diketone-cobalt complexes show a good inhibitory effect against tumor,and the inhibiting effect against rat C6 glioma cells at least partially via apoptosis.