依达拉奉对氯胺酮致PC12细胞凋亡时线粒体功能的影响  

Effect of edaravone on mitochondrial function during ketamine-induced apoptosis in PC12 cells

作　　者：司建洛[1] 杨木强[1] 张洪军[1] 苗亚飞 Si Jianluo;Yang Muqiang;Zhang Hongjun;Miao Yafei(Department of Anesthesiology,the First Affiliated Hospital of Henan University of Science and Technology,Luoyang 471003,China)

机构地区：[1]河南科技大学第一附属医院河南科技大学临床医学院麻醉科,洛阳471003

出　　处：《中华麻醉学杂志》2021年第9期1101-1104,共4页Chinese Journal of Anesthesiology

摘　　要：目的评价依达拉奉对氯胺酮致PC12细胞损伤时线粒体功能的影响。方法将神经生长因子诱导分化的PC12细胞采用随机数字表法分为3组(n=30):对照组PC12细胞正常培养;氯胺酮组PC12细胞诱导分化后第7天加入PBS+100μmol/L氯胺酮培养;依达拉奉+氯胺酮组加入10μmol/L依达拉奉+100μmol/L氯胺酮培养。于培养24 h时采用试剂盒测定细胞活力、caspase-3/7活性、ROS活性、ATP含量和NADH/NAD^(+)比例,TUNEL法观察细胞凋亡情况,计算细胞凋亡率。结果与对照组比较,氯胺酮组和依达拉奉+氯胺酮组细胞活力、caspase-3/7活性、NADH/NAD^(+)比例和细胞凋亡率升高,ROS活性和ATP含量降低(P<0.05);与氯胺酮组比较,依达拉奉+氯胺酮组细胞活力、caspase-3/7活性、NADH/NAD^(+)比例和细胞凋亡率降低,ROS活性和ATP含量升高(P<0.05)。结论依达拉奉抑制氯胺酮致PC12细胞凋亡的机制与其改善线粒体功能有关。Objective To evaluate the effect of edaravone on mitochondrial function during ketamine-induced apoptosis in PC12 cells.Methods Nerve growth factor(NGF)-induced differentiating PC-12 cells were divided into 3 groups(n=30 each)using a random number table method:control group(group C),ketamine group(group K)and edaravone plus ketamine group(group EK).Cells in group C were commonly cultured.In group K,PC12 cells were incubated with PBS and 100μmol/L ketamine at 7 days after differentiation.In group EK,cells were incubated with 10μmol/L edaravone and 100μmol/L ketamine.The cell viability,caspase-3/7 activity,reactive oxygen species(ROS)activity,adenosine triphosphate(ATP)content and NADH/NAD^(+) ratio were determined using analysis kits at 24 h of incubation.The cell apoptosis was observed by TUNEL assay and apoptosis rate was calculated.Results Compared with group C,the cell viability,caspase-3/7 activity,NADH/NAD^(+) ratio and apoptosis rate were significantly increased,and ROS activity and ATP content were decreased in group K(P<0.05).Compared with group K,the cell viability,caspase-3/7 activity,NADH/NAD^(+) ratio and apoptosis rate were significantly decreased,and ROS activity and ATP content were increased in group EK(P<0.05).Conclusion The mechanism by which edaravone inhibits ketamine-induced apoptosis in PC12 cells is related to improving mitochondrial function.

关 键 词：依达拉奉 氯胺酮 线粒体功能障碍 

分 类 号：R965[医药卫生—药理学]