权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Neurorepair and functional recovery by motor exercise in rats after ischemia reperfusion

运动锻炼对大鼠缺血再灌注后的神经修复和功能恢复

基本信息

批准号：
23500590
负责人：
HARUTOSHI Sakakima
金额：
$ 3.33万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2011
资助国家：
日本
起止时间：
2011 至 2013
项目状态：
已结题

项目摘要

We examined whether exercise reduces brain infractions, decreases neuronal apoptotic cell death, and improves neurobehavioral functions via the PI3K/Akt dependentpathway using rat middle cerebral artery occlusion (MCAO) model.Motor exercise provided neuroprotection, reduced neuronal cell death, maintained tissue structure, and aided functional recovery by stimulating the expression of neurorepair mediators BDNF/pTrkB via activating Akt2). Because the benefit of exercise in neurorepair hasbeen linked with the activation of the PI3 kinase/Akt pathway, we used aselective PI3 kinase inhibitor LY to confirm this mechanism in our study.Exercise improved neurobehavioral functions, indicating that the reduced deficits are related with the exercise-mediated decreased neuronal apoptotic cell death. Early motor exercise aid functional recovery by stimulating neurorepair mechanisms after stroke.

我们利用大鼠大脑中动脉闭塞（MCAO）模型研究了运动是否通过PI3K/Akt依赖通路减少脑梗死，减少神经元凋亡细胞死亡，并改善神经行为功能。运动可以提供神经保护，减少神经元细胞死亡，维持组织结构，并通过激活Akt2来刺激神经修复介质BDNF/pTrkB的表达，从而帮助功能恢复。由于运动对神经修复的益处与PI3激酶/Akt通路的激活有关，我们在研究中使用选择性PI3激酶抑制剂LY来证实这一机制。运动改善了神经行为功能，表明减少的缺陷与运动介导的神经元凋亡细胞死亡减少有关。早期运动通过刺激中风后的神经修复机制来帮助功能恢复。