依达拉奉对H_2O_2诱导的HepG2细胞氧化应激损伤的保护作用Investigation the Protection Effects of Edarovane on H_2O_2 Induced Oxidative Stress in HepG2 Cells
陈荧,张亮
CHEN Ying,ZHANG Liang
摘要(Abstract):
目的研究依达拉奉对H_2O_2诱导HepG2细胞损伤的保护作用。方法以400μmol·L~(-1)的H_2O_2诱导HepG2细胞氧化应激损伤,MTT法测定细胞存活率,ELLSA法测定细胞中丙二醛(MDA)、总超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化物酶(GSH-PX)水平的变化。结果依达拉奉可降低H_2O_2引起的细胞凋亡和细胞内MDA表达水平,升高GSH-PX和T-SOD表达水平。结论依达拉奉对H_2O_2诱导的HepG2细胞氧化应激损伤有保护作用。
To investigate the protection effect of edarovane on H_2O_2 induced oxidative stress in HepG2 cells.METHODS An experimental HepG2 cell damage model induced by H_2O_2( 400μM) was established. Cell viability was measured by MTT assay. ELISA kits were used to measure GSH- PX,T-SOD activities and MDA content. RESULTS Edarovane effectively reduced the H_2O_2-induced apoptosis of HepG2 cells. Edarovane elevated the activities of superoxide dismutase( SOD) and glutathione peroxidase( GSH-PX),and the content of malondialdehyde( MDA) was decreased. CONCLUSION Edarovane shows the protection effects on H_2O_2 induced oxidative stress in HepG2 cells.
关键词(KeyWords):
依达拉奉;H2O2;氧化应激损伤;保护作用
edaravone;H2O2;oxidative stress injury;protection
基金项目(Foundation):
作者(Author):
陈荧,张亮
CHEN Ying,ZHANG Liang
参考文献(References):
- [1]Paniker N V,Srivastava S K,Beutler E.Glutathuone metabolism of the cells:Effect of glutathione reductase deficiency on the stimulation of hexose monophosphate shunt under oxidative stress[J].Biochem Biophys Acta,2014,215(3):456-60.
- [2]Halliwell B.Oxidants and human disease:some new concepts[J].AFSEBJ,2013,1:358-64.
- [3]Abe K,Yuki S,Kogure K.Strong attenuation of ischemic and Postischemic brain edema in rats by a novel free radical scavenger[J].Stroke,2014,19:480-485.
- [4]黄建敏,杜书章,张晓坚.依达拉奉在体外循环心脏手术患者中治疗心肌缺血再灌注损伤作用的Meta分析[J].药学与临床研究,2015,18(6):5 54-557.
- [5]Emerit J,Edeas M,Bricaire F.Neurodegenerative diseases and oxidative Stress[J].Biomed Pharmacother,2014,58(1):39-46.
- [6]Lin Y K,Zeng Y S,Qu Z Q,et al.Oxidative stress and Alzheimer's disease[J].Anato Res,2012,31:67-70.
- [7]Su Y T.The neurobiological pathogenesis of Alzheimer's disease and therapeutic research advances[J].J Clin Res,2013,28(5):947-950.