JAK2/STAT3信号通路在依达拉奉减轻大鼠小胶质细胞缺血再灌注损伤中的作用  

Role of JAK2/STAT3 signaling pathway in Edaravone inhibiting ischemic reperfusion injury of microglia in rats

作　　者：黄丁丁[1] 翁浩[1] 刘荣[1] 徐志勇[1] 刘海健[1] 

机构地区：[1]上海交通大学附属第六人民医院南院麻醉科,上海201400

出　　处：《中国医药导报》2016年第31期16-19,共4页China Medical Herald

基　　金：上海市卫生局青年科研项目(20114y138);上海市第六人民医院医疗集团科学研究项目(2014)

摘　　要：目的评价Janus激酶2/信号转导子和转录激活子3(JAK2/STAT3)信号通路在依达拉奉抑制大鼠小胶质细胞缺血再灌注损伤后脑损伤中的作用。方法体外培养SD乳鼠小胶质细胞,采用随机数字表法分为常规培养组(C组)、糖氧剥夺组(OGD组)、依达拉奉组(EDA组)。OGD组小胶质细胞糖氧剥夺6 h,再灌注12 h建立缺血再灌注损伤模型;EDA组细胞糖氧剥夺后加入含EDA(浓度50μmol/L)的正常培养基后处理12 h。采用CCK8法检测细胞存活率的变化;Western blot法检测JAK2蛋白磷酸化(p-JAK2)、STAT3蛋白磷酸化(p-STAT3)变化;ELISA法检测IL-1β和IL-6的变化;流式细胞仪检测细胞凋亡率。结果与C组比较,OGD组细胞存活率降低,p-JIK2和p-STAT3的表达上调,细胞上清液中IL-1β和IL-6浓度增加,细胞凋亡率增加,差异有统计学意义(P<0.05);与OGD组比较,EDA组细胞存活率增加,p-JAK2和p-STAT3表达下调,细胞上清液的IL-1β和IL-6浓度减少,细胞凋亡率降低,差异有统计学意义(P<0.05)。结论依达拉奉后处理抑制大鼠小胶质细胞缺血再灌注损伤后炎性反应和细胞凋亡与JAK2/STAT3信号通路部分相关。Objective To evaluate the effect of Janus kinase 2/signal transducers and activators of transcription 3（JAK2/STAT3） signaling pathway on Edaravone inhibiting brain injury after ischemia-reperfusion injury in rats.Methods Microglia cells of rats were cultured in vitro, and divided into 3 groups： normal culture group（group C）, oxygen glucose deprivation group（group OGD）, and Edaravone group（group EDA）. The ischemia model in vitro was induced by oxygen and glucose deprivation 6 h and reperfusion 12 h; group EDA received Edaravone（50 μmol/L） for 12 h after oxygen glucose deprivation. CCK-8 was used to test the cell viability. Western blot was used to detect the expression of phosphorylation of JAK2（p-JAK2） and STAT3（p-STAT3）. ELISA was used to detect the change of inflammatory mediators IL-1β and IL-6. Apoptosis of microglia was assayed by flow cytometry. Results Compared with group C, the cell survival rates decreased, the expression of p-JAK2 and p-STAT3 were significantly up-regulated, the contents of IL-1β, IL-6 increased, and the cell apoptosis rate increased in group OGD respectively, with statistically significant differences（P〈0.05）. Compared with group OGD, the cell survival rates increased, expression of p-JAK2 and p-STAT3 decreased, contents of IL-1β and IL-6 decreased, and the cell apoptosis rate decreased in group EDA respectively, with statistically significant differences（P〈0.05）. Conclusion Edaravone postprocessing inhibits inflammation and apoptosis of microglia after ischemia-reperfusion injury in rats related to JAK2/STAT3 signaling pathway.

关 键 词：依达拉奉 小胶质细胞 STAT3转录因子 脑损伤 

分 类 号：R332[医药卫生—人体生理学]