【摘要】 目的观察大鼠局灶性脑缺血/再灌注后丝裂原活化蛋白激酶家族中JNK1/2(c-Jun氨基末端激酶1/2)的活化情况以及银杏叶提取物Egb761对其影响。方法雄性成年SD大鼠随机分成3组(n=5):假手术组、生理盐水对照组和Egb761组。分别于缺血前6天每天用生理盐水4 m l和Egb761 150 mg/kg(Egb761用4 m l生理盐水溶解)灌胃。采用线栓法致大脑中动脉栓塞(MCAO)模型,在脑缺血再灌注后处死大鼠,对缺血侧海马进行免疫印迹法检测JNK1/2磷酸化水平。结果局灶脑缺血/再灌注可以诱导JNK1/2激活,30 m in达第1个高峰,3天达第2个高峰;Egb761可显著抑制脑缺血再灌注后JNK1/2的激活(P<0.05),JNK1/2的蛋白表达量在以上不同处理条件下没有明显变化。结论局灶性脑缺血再灌注可诱导缺血侧海马JNK1/2活化,Egb761干预可使缺血侧海马JNK1/2活化受到抑制,减轻缺血侧海马的损伤。更多还原

【Abstract】 Objective To investigate the activation of JNK1/2 induced by focal cerebral ischemia/reperfusion in rats and the effect of Egb761 on it.Methods Male adult SD rats were randomly divided into 3 groups(n=5 each),the sham-operation group,the vehicle control group and the Egb761 treatment group.The model of middle cerebral artery occlusion(MCAO) was established by thread ligation method before ischemia.The control rats were given intragastricly 4 ml of normal saline qd for 6 d and the Egb761treated rats were given intragastricly 150 mg/ kg of Egb761 dissolved in 4 ml of normal saline qd for 6 d.The rats were decapitated after reperfusion;the involved hippocampus was taken to assay the activation of JNK1/2 by Western blotting.Results The activation of JNK1/2 was induced by focal cerebral ischemia,reaching its first peak at 30 min of reperfusion and the second peak on 3 d.Egb761 evidently inhibited the JNK1/2 activation(P<0.05).The level of JNK1/2 protein was rather steady in spite of the ways of pre-ischemic treatment in the 3 groups.Conclusion Focal cerebral ischemia/reperfusion induces JNK1/2 activation in the ischemic hippocampus;Egb761 can inhibit the activation and alleviate the ischemic injury in the ischemic hippocampus.更多还原