依达拉奉对大鼠脑缺血模型MAPK表达的影响  

Effect of Edaravone on the MAPK Pathways after Brain Ischemia in Rats

作　　者：孙德标[1] 胡海涛[1] 

机构地区：[1]浙江大学医学院附属第二医院,310009

出　　处：《心脑血管病防治》2012年第4期294-296,303,共4页CARDIO-CEREBROVASCULAR DISEASE PREVENTION AND TREATMENT

摘　　要：目的探讨自由基清除剂依达拉奉对大鼠脑缺血后丝裂原激活的蛋白激酶(MAPK)表达的影响。方法大脑中动脉阻断法制备大鼠脑缺血再灌注模型,缺血60min后再灌注23h,术前30min及再灌注2h时尾静脉注射依达拉奉1.0mg.kg-1或0.9%氯化钠注射液2ml.kg-1。观察大鼠脑缺血后神经功能缺损症状,TTC染色法检测梗死体积,Fluoro-Jade C法检测细胞死亡,采用免疫印迹法检测MAPK家族三个主要成员:蛋白激酶P38(P38 MAPK),细胞外信号调节激酶(ERK1/2)和c-jun氨基末端激酶(JNK)的表达。结果依达拉奉改善大鼠脑缺血再灌注23h后神经功能缺损症状,减少梗死体积和细胞死亡(P<0.05);大鼠脑缺血后MAPK家族被激活(P<0.01),依达拉奉能显著降低P38MAPK和JNK的激活,但对ERK1/2的表达无明显影响。结论依达拉奉可能能够通过抑制脑缺血后细胞内P38MAPK和JNK信号传导通路,减轻大鼠脑缺血损伤。Objective To investigate the effect of Edaravone, a free radical scavenger, on mitogen activated prolein kinase（MAPK） pathways after cerebral ischemia in rats. Methods Focal cerebral ischemia was induced by 60rain of middle cerebral artery （MCA） occlusion and followed by 23h reperfusion. Edaravone （ 1.0mg·kg- 1 ） or vehicle （ saline 2 ml·kg - l ） was intravenously injected 30rain belore MCA occlusion and 2h after reperfusion. The neurological score was observed via comer test. Infarct volume, neuron death in hippocampus was determined using an image analyzer, lree major members of MAPK family： P38 MAPK, extracellular reg- ttlated kinase 1/2（ERK1/2） and C-Jnn NH2-tenninal kinase （JNK） were analyzed by western blot. Results Edaravone improved the neurological deficits, and decreased infarct volume and neuron death （ P 〈 0.05）. MAPK f^mtily was activated afler brain ischemia （ P 〈 0.01 ）. Edaravone could reduce phosphorylation of JNK and P38 MAPK whereas there was no obviously effect on phospholyla- tion of ERK1/2. Conclusions Edaravone probably inhibits P38 MAPK and JNK pathways to attenuate the damage induced by brain is- chemia in rats.

关 键 词：依达拉奉 脑缺血/再灌注 丝裂原激活的蛋白激酶(MAPK) 

分 类 号：R743.3[医药卫生—神经病学与精神病学]