【打印本页】 【下载PDF全文】 【HTML】 查看/发表评论下载PDF阅读器关闭

←前一篇|后一篇→

过刊浏览    高级检索

本文已被:浏览 67次   下载 17 本文二维码信息
码上扫一扫!
迷走神经电刺激对急性缺血性脑卒中大鼠继发性脱髓鞘的影响
王思思,郑富荣,王三荣,贾功伟*
0
(重庆医科大学附属第二医院康复科, 重庆 400010
*通信作者)
摘要:
目的 采用大鼠脑缺血再灌注(I/R)模型观察缺血性脑卒中后非缺血侧胼胝体髓鞘的变化规律,并探讨迷走神经电刺激(VNS)对I/R模型继发性脱髓鞘的影响。方法 选取42只大鼠随机分为假手术组、I/R组、I/R+VNS组,每组14只。除假手术组外,其他组大鼠均采用大脑中动脉阻塞线栓法构建I/R模型,同时I/R+VNS组大鼠在缺血阻塞后30 min予左侧迷走神经60 min重复电刺激。采用2,3,5-氯化三苯基四氮唑染色观察脑梗死体积,采用蛋白质印迹法检测非缺血侧胼胝体中髓鞘碱性蛋白(MBP)、髓鞘相关糖蛋白(MAG)的表达水平,采用固蓝染色和透射电子显微镜分别观察非缺血侧胼胝体髓鞘完整性和髓鞘厚度。结果 与假手术组相比,I/R组脑梗死体积增大(P<0.01)。I/R后第3天,与假手术组相比,I/R组大鼠非缺血侧胼胝体MBP、MAG蛋白表达水平下降(均P<0.01),固蓝染色强度降低(P<0.01),髓鞘厚度变薄(g-ratio增高,P<0.01);而与I/R组相比,I/R+VNS组大鼠非缺血侧胼胝体MBP、MAG表达水平升高(均P<0.05),固蓝染色强度增加(P<0.01),髓鞘厚度增加(g-ratio下降,P<0.01)。结论 缺血性脑卒中后大鼠非缺血侧胼胝体发生继发性脱髓鞘改变,VNS可改善继发性脱髓鞘改变。
关键词:  脑卒中  缺血再灌注损伤  迷走神经电刺激  胼胝体  继发性脱髓鞘
DOI:10.16781/j.CN31-2187/R.20240541
投稿时间:2024-08-01修订日期:2024-12-10
基金项目:国家自然科学基金面上项目(82472616),重庆市科卫联合医学科研面上项目(2021ZY023818).
Effect of vagus nerve stimulation on secondary demyelination in rats with acute ischemic stroke
WANG Sisi,ZHENG Furong,WANG Sanrong,JIA Gongwei*
(Department of Rehabilitation Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China)
Abstract:
Objective To observe the changes of myelin sheath in corpus callosum on non-ischemic side after ischemic stroke in rats with cerebral ischemia/reperfusion (I/R) model, and to investigate the effect of vagus nerve stimulation (VNS) on secondary demyelination in I/R model. Methods Forty-two rats were randomly assigned to sham, I/R, or I/R+VNS groups, with 14 rats in each group. Except for the sham group, the rats in other groups were used to construct I/R model by a middle cerebral artery occlusion thread method. In addition, the rats in the I/R+VNS group were given repetitive electrical stimulation of the left vagus nerve for 60 min at 30 min after ischemia occlusion. The cerebral infarction volume was observed by 2,3,5-triphenyltetrazolium chloride staining. The expression levels of myelin basic protein (MBP) and myelin-associated glycoprotein (MAG) in the corpus callosum on the non-ischemic side were detected by Western blotting. The integrity and thickness of myelin sheaths in the corpus callosum on the non-ischemic side were observed by Luxol fast blue staining and transmission electron microscopy, respectively. Results Compared with the sham group, the volume of cerebral infarction in the I/R group was increased (P<0.01). On the 3rd day after I/R, compared with the sham group, the expression levels of MBP and MAG were significantly decreased (both P<0.01), the intensity of Luxol fast blue staining was significantly decreased (P<0.01), and the thickness of the myelin sheath was significantly thinner (g-ratio was increased, P<0.01) in the corpus callosum on the non-ischemic side. Compared with the I/R group, the expression levels of MBP and MAG in the I/R+VNS group were significantly increased (both P<0.05), the intensity of Luxol fast blue staining was significantly increased (P<0.01), and the thickness of myelin sheath was significantly increased (g-ratio was decreased, P<0.01) in the corpus callosum on the non-ischemic side. Conclusion Secondary demyelination occurs on the non-ischemic side of the rat corpus callosum after ischemic stroke, and VNS can ameliorate the demyelination.
Key words:  stroke  ischemia/reperfusion injuries  vagus nerve stimulation  corpus callosum  secondary demyelination