抗霉素A抑制PC12细胞线粒体COⅡ基因表达  

ANTIMYCIN A INHIBIT THE EXPRESSION OF MITOCHONDRIAL COⅡ GENE IN PC12 CELLS

作　　者：邱小忠[1] 欧阳钧[1] 余磊[1] 张黎声[1] 陆云涛[1] 陈瑗[1] 周玫[1] 钟世镇[1] 

机构地区：[1]第一军医大学临床解剖学研究所,广州510515

出　　处：《神经解剖学杂志》2004年第2期167-170,共4页Chinese Journal of Neuroanatomy

摘　　要：采用不同浓度的抗霉素 A(一种能提高线粒体内活性氧水平的线粒体抑制剂 )处理 PC12细胞 ,利用血细胞计数、台盼蓝排除法以及 MTT法进行细胞活性检测。实验证明 ,当抗霉素 A的浓度达到 15 0 μmol/L时 ,PC12细胞开始出现损伤 ;进一步采用 RNA斑点杂交和 RT-PCR技术分析发现抗霉素 A所致的细胞损伤和线粒体内细胞色素 C氧化酶亚基 (CO )基因表达下降有关。本研究证实线粒体介导的活性氧的产生能早期诱导线粒体细胞色素氧化酶的活性的改变 ,逐步引起PC12 cell line was treated with different concentrations of antimycin A, a mitochondrial inhibitor that increases the release of mitochondrial ROS. Cell number was counted by hemocytometer and cell viability was determined by the trypan blue exclusion method. Cell viability was also monitored by MTT assay. It was found that while cells treated with low doses of 150 mmol/L antimycin A,damages appeared in the PC12 cell lines. We also found that the change of expression lever of COⅡ gene was linked to the damage of cells induced by antimycin A through RT PCR and dot blotting analysis. The results suggest that increased production of mitochondrial ROS can alter the activity of COⅡ originally and induce cell apoptosis step by step.

关 键 词：抗霉素A PCI2细胞 线粒体 COⅡ 基因表达 细胞色素C氧化酶亚基Ⅱ 活性氧 损伤 

分 类 号：R361[医药卫生—病理学]