D-氨基葡萄糖衍生物诱导Eca-109细胞凋亡的机制  

Effect of derivatives of D-aminoglucose on the reactive oxygen species and mitochondrial membrane ptoential change of Eca-109 cells

作　　者：吴静[1,2] 杨国栋[2,4] 路红[2] 强占荣[2] 周永宁[2] 王爱勤[3] 薛群基[3] 

机构地区：[1]北京世纪坛医院,北京大学第九临床医学院消化科,北京100038 [2]兰州大学第一医院消化科,甘肃兰州730000 [3]中国科学院兰州物理化学研究所,甘肃兰州730000 [4]川北医学院附属医院消化科,四川南充637000

出　　处：《中国药理学通报》2008年第1期33-36,共4页Chinese Pharmacological Bulletin

基　　金：中国科学院西部之光资助项目(NoCX805)

摘　　要：目的探讨2-(3-羧基-1-丙酰氨基)-2-脱氧-D-葡萄糖{2-[(3-carboxy-1-oxoprogy1)amino]-2-deoxy-D-Glucose,CO-PADG}诱导Eca-109细胞凋亡的机制。方法不同浓度COPADG作用于人食管癌Eca-109细胞24h,检测Eca-109细胞的抑制率、凋亡率、细胞内活性氧(reactive oxygen spe-cies,ROS)、线粒体跨膜电位。结果Eca-109细胞凋亡率与COPADG浓度呈正相关,r=1.0,P<0.01;Eca-109细胞线粒体膜电位水平与Eca-109细胞凋亡率相关,r=1.0,P<0.01;ROS水平与Eca-109细胞凋亡率呈正相关,r=1.0,P<0.01;ROS水平与Eca-109细胞线粒体膜电位水平呈负相关,r=1.0,P<0.01。结论COPADG可促进Eca-109细胞凋亡,提高Eca-109细胞内ROS水平,并降低线粒体膜电位。实验结果提示COPADG提高ROS,降低Eca-109细胞线粒体膜电位启动细胞凋亡通路促使Eca-109细胞凋亡,并且线粒体膜电位的下降是通过提高ROS实现的。Aim To study the mechanism of COPADG induced apoptosis of Eca-109 cells. Methods Eca- 109 cells were cultured with different densiiy COPADG 24 h, then cell growth inhibitory rate, apoptotic rate, ROS, △ψm of Eca-109 cells were examined. Results The apoptotic rate of Eca-109 cells and the COPADG density presented positively related, r = 1.0,P 〈0. 01 ; △ψm and the apoptotic rate of Eca-109 cells were neg- atively related,r = 1.0,P 〈0. 01 ; ROS and the apoptotic rate presented positively related, r = 1.0, P 〈 0.01 ; ROS and △ψm were negatively related,r = 1.0,P 〈0. 01. Conclusions COPADG can promote apoptosis of Eca-109 cells, raise ROS level inside Eca-109 cells and also lower △ψm PADG increases ROS and The experiment hints COlowers the △ψm combined with the start of cell apoptosis thoroughfare to induce apoptosis of Eca-109 cells. The increase of ROS can lead to the descent of △ψm.

关 键 词：2-(3-羧基-1-丙酰氨基)-2-脱氧-D-葡萄糖 人食管癌 ECA-109细胞 凋亡 活性氧 细胞线粒体跨膜电位 

分 类 号：R329.24[医药卫生—人体解剖和组织胚胎学] R329.25[医药卫生—基础医学]