电刺激迷走神经对大鼠脑缺血后轴突再生及RGMa表达的影响  

Effects of Vagus Nerve Stimulation on Axonal Regeneration and RGMa Expression in Rat Focal Cerebral Ischemia Reperfusion Models

作　　者：程创[1] 侯良绢[1] 冯晓灵[1] 陈元武 郎俊峰 石中全[1] Cheng Chuang;Hou Liangjuan;Feng Xiaoling;Chen Yuanwu;Lang Junfeng;Shi Zhongquan(Chongqing Three Gorges Medical College,Chongqing,404120)

机构地区：[1]重庆三峡医药高等专科学校,重庆404120

出　　处：《基因组学与应用生物学》2020年第4期1867-1872,共6页Genomics and Applied Biology

基　　金：重庆市教育委员会科学技术研究项目(No.KJ1725382)资助。

摘　　要：本研究拟探讨电刺激迷走神经对大鼠脑缺血/再灌注(I/R)损伤后轴突再生和排斥性导向因子A(RGMa)蛋白表达的影响。首先,准备成年雄性SD(Sprague-Dawley)大鼠36只,并随机分成假手术组(Sham组)、脑缺血/再灌注组(I/R组)和迷走神经电刺激组(I/R+VNS组)。随后,构建大脑中动脉阻塞(MCAO)模型,并进行右侧颈部迷走神经电刺激,然后进行神经功能评分,通过Western blotting法检测迷走神经电刺激对脑缺血侧皮质和海马组织中RGMa表达的影响,利用免疫组织化学实验检测迷走神经电刺激对脑缺血侧皮质和海马组织细胞中RGMa和轴突生长标记神经微丝蛋白200(NF200)蛋白表达的影响。与I/R组相比,迷走神经电刺激可以明显改善神经功能(p<0.01);与Sham组相比,I/R组脑缺血侧皮质和海马中NF200蛋白表达明显降低(p<0.01),而RGMa蛋白的表达明显增加(p<0.01);与I/R组相比,迷走神经电刺激处理组脑缺血侧皮质和海马中NF200蛋白表达明显升高(p<0.05),而RGMa蛋白的表达明显降低(p<0.01)。上述结果表明电刺激迷走神经可以明显改善大鼠脑缺血/再灌注损伤后神经功能缺失,其机制可能与抑制RGMa表达进而促进轴突再生有关。To determine the effects of vagus nerve stimulation(VNS)on the neurological function deficit,axonal regeneration and repulsive guidance molecule A(RGMa)expression in rat cerebral ischemia reperfusion,thirty-six Sprague-Dawley(SD)rats were randomly divided into three groups:sham group,cerebral ischemia reperfusion group(I/R)and vagus nerve stimulation group(I/R+VNS).Firstly,rat middle cerebral artery occlusion(MCAO)models were performed.Secondly,rats were treated with VNS.Then the neurological function deficit was evaluated.The effect of VNS on RGMa protein expression was determined by Western blotting assay and immunohistochemistry assay.The axonal regeneration was determined by neurofilament 200(NF200)immunohistochemistry assay.Compared with I/R group,VNS treatment significantly ameliorated I/R-induced neurological deficit(p<0.01).Compared with sham group,I/R significantly repressed the expression of NF200 protein and induced the expression of RGMa protein in ischemic cortex and hippocampus.Compared with I/R group,VNS treatment significantly increased the expression of NF200 protein and inhibited the expression of RGMa protein in ischemic cortex and hippocampus.These results suggest that VNS ameliorates I/R-induced neurological deficit,which may be due to the inhibition of RGMa protein expression level and inducing axonal regeneration.

关 键 词：迷走神经电刺激 RGMa NF200 轴突再生 

分 类 号：R743.3[医药卫生—神经病学与精神病学]