脑红蛋白在脑梗死大鼠脑组织中的表达及其神经保护作用机制  

Expression of neuroglobin in brain tissue of rats with cerebral infarction and its neuroprotective mechanisms

作　　者：张蓓[1] 李亚军[1] 张世俊[1] 任会云 王敏娟[1] 郭长江[1] 

机构地区：[1]西安医学院附属医院神经内科,陕西西安710077

出　　处：《吉林大学学报（医学版）》2012年第6期1114-1118,共5页Journal of Jilin University：Medicine Edition

基　　金：陕西省自然科学基金资助课题(2010JM4054);陕西省教育厅科研基金资助课题(09JK713)

摘　　要：目的:观察脑梗死大鼠脑组织中脑红蛋白(Ngb)的表达及其对PI3K/Akt信号通路的影响,探讨二者在缺血性脑损伤中的作用及Ngb神经保护作用的可能机制。方法:60只SD大鼠随机分为假手术组、缺血组、Hemin(Ngb诱导剂)组、LY(PI3-K/Akt抑制剂LY294002)组和Hemin+LY组,每组12只。应用大脑中动脉线栓法制备脑梗死动物模型,术后24h观察各组大鼠神经功能评分和脑组织梗死体积;应用RT-PCR法检测各组大鼠脑组织Ngb mRNA表达水平及PI3-K/Akt活性。结果:假手术组未见TTC不着色区,未检出神经功能缺损。与缺血组比较,Hemin组大鼠脑组织中Ngb和Akt mRNA表达水平升高(P<0.01),神经功能评分降低(P<0.05),脑梗死体积减小(P<0.01);与缺血组比较,LY组大鼠脑梗死体积增加(P<0.01),神经功能评分升高(P<0.05),Akt mRNA表达水平降低(P<0.01),Ngb无明显变化。与Hemin组比较,Hemin+LY组大鼠脑组织损伤加重,Akt mRNA表达水平明显降低(P<0.01),Ngb未被抑制。结论:Ngb可以减小局灶性脑缺血大鼠脑梗死体积,改善神经功能,并且可能通过PI3K/Akt信号通路发挥神经保护作用。Objective To observe the expression of neuroglobin（Ngb）in brain tissue of rats with cerebral infarction and its effect on PI3-K/Akt signaling pathway,and to study their effects on cerebral ischemic injury and the possible mechanisms of the neuroprotective effect of Ngb.Methods 60 SD rats were randomly divided into sham operation group,ischemia group,and Hemin group,LY group,and Hemin＋LY group,and there were 12 rats in each group.Cerebral infarction models were established by middle cerebral artery thread embolism method.All rats were sacrificed 24 h after operation for neurological evaluation and detection of cerebral infarction volume,and the expression levels of Ngb and Akt mRNA were detected by RT-PCR.Results There was not any area unstained by triphenyltetrazolium chloride and any neurologic impairment found in rats in sham operation group.Compared with ischemia group,the expression levels of Ngb and Akt mRNA in Hemin group were increased significantly（P0.01）,with better neurological function（P0.05） and less volume of cerebral infarction（P0.01）.The volume of cerebral infarction（P0.01） and the neurological impairments（P0.05）in LY group were increased,and the expression level of Akt mRNA in LY group was lower（P0.01）than that in ischemia group,and there was no significant difference in the expression of Ngb（P0.05）.The cerebral tissue damage in Hemin＋LY group was aggrevated,and the expression level of Akt mRNA was decreased（P0.01）,while the level of Ngb mRNA was not inhibited by LY294002（P0.05） compared with Hemin group.Conclusion Ngb can reduce the volume of cerebral infarction and improve neurological function after focal cerebral ischemia in rats and its neuroprotective effect may be realized by activating PI3-K/Akt signaling pathway.

关 键 词：脑红蛋白 磷脂酰肌醇-3激酶 丝氨酸-苏氨酸蛋白激酶 脑梗死 

分 类 号：R743.33[医药卫生—神经病学与精神病学]