Protection of edaravone no the rat microglia after ischemia reperfusion

Objective To evaluate the Janus kinase2/signal transducers and activators of transcription 3(JAK2/STAT3) signaling pathway on edaravone inhibiting inflammatory reaction after ischemia-reperfusion injury in rats. Methods Cultured Sprague-Dawley rats microglia in vitro,using the random number table method,microglia were divided into 3 groups(n=20 each):normal culture group(group C);Glutamate group(group Glu);edaravone group(group Eda);Microglia in group Glu and group Eda exposed to medium containing 1 mmol/L Glu for 30 min.Microglia cell were treated with 100 μmol/L edaravone after glutamate neurotoxicity in group Eda.The CCK8 assay was used to detect the changes in cell viability.Real time quantitative PCR technique was used to the level of JAK2 STAT3 mRNA,ELASA was used to detect the changes of inflammatory mediators;Apoptosis of microglia was assayed by flow cytometry. Results Compared with group C,cell survival rates in group Glu decreased,and the expression of JAK2 and STAT3 mRNA were up-regulated,and the contents of TNF-α,IL-2 were increased,and the cell apoptosis rate increased,respectively(P<0.05);Compared with group Glu,the cell survival rates increased in group Eda,and expression of JAK2 and STAT3 mRNAdecreased in group Eda,and contents of TNF-α and IL-2 were decreased,and cell apoptosis rate decreased in group Eda,respectively(P<0.05). Conclusion Edaravone post-processing inhibits inflammatory cytokine expression of the rat microglia after ischemia and reperfusion injury related toJAK2/STAT3 signaling pathway.