摘要
该文研究氧化苦参碱（oxymatrine,OMT）抑制H2O2诱导的L02细胞损伤的作用及其机制。以人正常肝实质细胞L02为研究对象,采用H2O2诱导氧化应激建立肝损伤模型进行实验,通过CCK-8检测OMT对L02细胞活性的影响;CSFE荧光实验检测OMT对L02细胞增殖的影响;流式细胞术检测OMT对H2O2诱导的L02细胞凋亡率的影响;DCFH-DA荧光探针检测OMT对H2O2诱导的L02细胞内ROS含量;微板比色法检测OMT对GSH-PX和SOD活性的影响。结果显示,OMT在6.25~100 mg·L-1通过诱导NADPH的产生,增强L02细胞内GSH-PX酶和SOD酶的活性,进而促进GSH介导的活性氧ROS的清除,从而抑制H2O2诱导的L02细胞凋亡的发生,达到抑制H2O2诱导L02细胞损伤的作用。
To investigate the protective effects of oxymatrine（ OMT） against H2O2-induced damage in L02 cells and research the mechanism,L02 cells were used as the research object. The oxidative stress model of L02 was established by hydrogen peroxide（ H2O2）. CCK-8 was used to detect the cell activation of L02 cells treated by different OMT. FCM（ flow cytometry） assay was used to evaluate the cell proliferation of L02 cells treated by OMT. The apoptosis of L02 cells was detected using Annexin-V /7-AAD apoptosis detection kit. The level of ROS was detected by DCFH-DA fluorescence probe. The GSH-PX and SOD were detected by micro plate and colorimetric method. Results showed that when the concentration of OMT is between 6. 25 and 100 mg·L- 1,it could promote the production of NADPH and strengthen the activity of GSH-PX and SOD to get rid of the ROS to protect the L02 cell from the apoptosis of L02 cell induced by H2O2.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2016年第7期1302-1307,共6页
China Journal of Chinese Materia Medica
基金
国家自然科学基金项目(813300486)
