Effect of Edaravone on Oxidative Stress Injury in HT22 Cells Injury by Regulating JAK2/STAT3 Signaling Pathway
Objective To investigate the effect of edaravone(EDA)on the oxidative stress injury in HT22 mouse hippocampal neurons.Methods HT22 cells were cultured in sugar-free medium at 37℃,1％O2,5％CO2,and 94％N2 for 8 h,the above medium was then discarded and a complete medium containing the drug was added,and HT22 cells were reoxygenated in a normal oxygen environment for 6 h to construct an oxidative stress injury cell model.HT22 cells were divided into the model group(complete medium),the EDA group(complete medium containing 1 mmol/L ED A),and the control group(continuously cultured under normal gas condition).The CCK-8 method was used to detect cell survival,and the cell survival rate was calculated;the lactate dehydrogenase(LDH),superoxide dismutase(SOD),and malondialdehyde(MDA)levels in cells were detected;the flow cytometry was used to detect cell apoptosis,and the apoptosis rate was calculated;the Western blot was used to detect the expression levels of Janus kinase 2(JAK2),signal transducer and activator of transcription 3(STAT3),phosphorylated-Janus kinase 2(p-JAK2),and phosphorylated-signal transducer and activator of transcription 3(p-STAT3).Results Compared with those in the model group,the cell survival rate significantly increased,cell apoptosis rate significantly decreased,LDH and MDA levels significantly decreased(P＜0.01),SOD level significantly increased,p-JAK2/JAK2 and p-STAT3/STAT3 significantly decreased in the EDA group(P＜0.01).Conclusion EDA has a obvious protective effect on the oxidative stress injury induced by oxygen-glucose deprivation/reperfusion in HT22 cells,and its mechanism may be related to the inhibition of the JAK2/STAT3 signaling pathway.
万方数据
维普
