中国药理学通报2012，Vol.28Issue(2)：255-260,6.DOI:10.3969/j.issn.1001-1978.2012.02.024
BAPTA-AM对MDCK细胞的保护作用及其机制
Protective effects of BAPTA-AM on D-GalN induced apoptosis in MDCK cells
施水娟 1宋必卫1
作者信息
- 1. 浙江工业大学药学院,浙江,杭州,310014
- 折叠
摘要
Abstract
Aim To investigate the protective effects and its mechanism of BAPTA-AM on D-GalN induced apoptosis in MDCK cells. Methods MDCK cells were pretreated with BAPTA-AM at concentrations ranged from 0.5 to 50 nmol · L-1 and followed the D-GalN (20 mmol · L-1 ) attack. The viabilities of MDCK cells were measured by MTT assay. Cell apoptosis was evaluated by Annexin V-EGFP/PI or Hoechst 33342/ PI labeling methods. Mitochondrial membrane potential ( Δψm ), Caspase-8, -9 were also tested to explore the inhibitory mechanisms. Results D-GalN attack resulted in MDCK cell injury characterized by the decrease of the cell viability, cell death ( especially apoptosis ), collapse of mitochondrial membrane potential, and the activation of Caspase-8 and Caspase-9. BAPTA-AM could significantly protect the cells against the injuries induced by D-GalN attack in a dose-dependnt manner. In addition,BAPTA-AM could markedly inhibit MDCK cell injury by intracellular calcium overload induced by A23187/CaCl2 and attenuate intracellular free Ca level ([ Ca2+ ]i ). Conclusion BAPTA-AM is a promising MDCK cell protector against D-GalN and A23187/CaCl2 induced injuries. Its mechanism of action is related to the decreasing [ Ca2+ ]i and in turn, protection of mitochondria and down-modulation of ap-optotic signal pathways.关键词
BAPTA-AM/MDCK细胞/线粒体/Caspase-8/Caspase-9/A23187/细胞凋亡Key words
BAPTA-AM/ MDCK cell/ mitochondria/Caspase-8/ Caspase-9/ A23187/ apoptosis分类
医药卫生引用本文复制引用
施水娟,宋必卫..BAPTA-AM对MDCK细胞的保护作用及其机制[J].中国药理学通报,2012,28(2):255-260,6.
