中国动脉硬化杂志2012，Vol.20Issue(4)：304-308,5.
依达拉奉保护H9c2心肌细胞对抗化学性低氧引起的损伤
Edaravone Protects H9c2 Cells Against Chemical Hypoxia-Induced Injury
摘要
Abstract
Aim To explore whether edaravone(EDA), a novel free radical scavenger, protect H9c2 cells against chemical hypoxia-indueed injury. Methods H9c2 cells were treated with Cobalt chloride (CoCl2) to set up a chemical hypoxia-induced cellular injury model. Cell viability was detected by cell counter kit (CCK-8). Changes in morphology and amount of apoptotic cells were observed by Hoechst 33258 staining; Intracellular level of reactive oxygen species (ROS) was measured by DCFH-DA staining and photofluorography, Mitochondrial membrane potential (MMP) was tested by JC-1 staining and photofluorography. Results Exposure of H9c2 cells to 100 -1000 ujnol/L CoClj for 24 h dose-dependently reduced cell viability. At the range from 12 to 36 h, 800 pjnol/L CoCl2 time-dependenlly inhibited cell viability. Pre-treatment with 10 to 40 ujnoI/L EDA or with NAC (a ROS scavenger) at 500 to 2000 ujnol/Lforl h prior to exposure to 800 ujnol/L CoCl2 for 24 h dose-dependently blocked the inhibition of cell viability by CoCl2. Preconditioning with 40 ujnol/L EDA for 1 h prior to exposure of H9c2 cells to 800 pjnol/L CoCl: inhibited not only CoClj-induced overproduction of ROS, but also the apoptotic effect and MMP loss induced by Cod,. Conclusions EDA can protect H9c2 cells against CoClj-induced injury, which may be associated with its antioxidant effect and protection of MMP.关键词
依达拉奉/H9c2心肌细胞/化学性低氧/活性氧/线粒体膜电位Key words
Edaravone/H9c2 Cells/Chemical Hypoxia/Reactive Oxygen Species/Mitochondrial Mem brane Potential分类
医药卫生引用本文复制引用
张蔼玲,兰爱平,郑东诞,胡芬,郭润民,沈宁,冯鉴强,廖新学..依达拉奉保护H9c2心肌细胞对抗化学性低氧引起的损伤[J].中国动脉硬化杂志,2012,20(4):304-308,5.基金项目
广东省科技计划项目(2011B080701051 （）
2010B080701105 （）
2009B08070104 （）
2007B080701030) （）
