维生素C诱导人宫颈癌Caski细胞凋亡及其分子机制的研究  

Molecular Mechanism of Vitamin C on Proliferation and Apoptosis of Human Cervical Cancer Cell Lines Caski in vivo

作　　者：杨建林[1] 韩钰[1] 周永芹[1] 张伟[1] 

机构地区：[1]三峡大学分子生物学研究所,中国湖北宜昌443002

出　　处：《生命科学研究》2013年第2期143-147,共5页Life Science Research

基　　金：三峡大学青年科学基金资助项目(KJ2008A038)

摘　　要：为了研究维生素C对人宫颈癌Caski细胞体外抑制、诱导凋亡的作用及其分子机制,使用不同剂量维生素C处理人宫颈癌Caski细胞,采用噻唑蓝(MTT)法检测药物对细胞增殖的抑制作用;流式细胞仪检测Cas-ki细胞周期变化;琼脂糖电泳法观察凋亡细胞DNA Ladder现象;Western blot检测凋亡相关蛋白Bcl-2、Bax和E6的表达以及Caspase 3的激活;荧光染色观察细胞线粒体膜电位的改变.分析发现,维生素C可显著抑制人宫颈癌Caski细胞增殖,呈现明显的时间和剂量依赖性;将细胞阻滞于S期;诱导细胞凋亡,下调Bcl-2和E6、上调Bax蛋白表达,促进Caspase3活化,降低线粒体膜电位.表明维生素C在体外可有效抑制人宫颈癌Caski细胞增殖,诱导细胞凋亡.To study the effects of Vitamin C on proliferation and apoptosis of human cervical cancer cell lines Caski in vivo. Caski cell was treated with different concentrations of Vitamin C in vitro. MTT was used for the analysis of cell proliferation, the flow cytometry was performed to assay cell cycles and DNA fragmentation assay was used to identify apoptotic cells, Western blot was used to evaluate the expression of apoptosis-related protein Bcl-2, Bax, E6 and Caspase 3, fluorescent dye assay was performed to determine the changes in mitochondrial membrane potential. Vitamin C treatment inhibited the proliferation of Caski cells significantly in a dosage- and time-dependent manner. The results from flow cytometry analysis indicated that Vitamin C interfered with cell cycles and increased cell percentage in S phase, at the same time, the number of apoptotic cells increased significantly. After Vitamin C treatment, the typical phenomenon for apoptotic cells was observed and the contents of pro-apoptotic protein Bax in the cytosol were significantly increased, but the contents of anti-apoptotic protein Bcl-2 and E6 and caspase 3 were down-regulated. Vitamin C accompanied by a significant reduction in the mitochondrial membrane potential in Caski cells. The results showed that the Vitamin C inhibits growth and induces apoptosis of Caski cell lines.

关 键 词：维生素C CASKI细胞 凋亡机制 

分 类 号：R542.220.5[医药卫生—心血管疾病]