白质
小胶质细胞
髓鞘碱性蛋白
神经炎症
医学
莫里斯水上航行任务
髓鞘
假手术
海马体
冲程(发动机)
免疫印迹
内科学
认知缺陷
内分泌学
病理
麻醉
中枢神经系统
炎症
认知障碍
生物
磁共振成像
放射科
生物化学
替代医学
疾病
工程类
基因
机械工程
作者
Yong Guo,Mei Yuan,Yu Han,Xiaoping Shen,Zhen-Kun Gao,Xia Bi
标识
DOI:10.1016/j.neuint.2022.105295
摘要
White matter damage is an important contributor to cognitive impairment after stroke. This study was designed to explore the beneficial effects of enriched environment (EE) on white matter recovery and cognitive dysfunction after stroke, and further explore the potential mechanism of EE on white matter recovery from the perspective of microglia and microglia-mediated neuroinflammation.Male SD rats underwent middle cerebral artery occlusion (MCAO) or sham surgery. During the MCAO operation, a laser Doppler blood flow meter was used to monitor the blood flow to ensure the success of the model. At 72 h after the operation, 3 rats were selected for TTC staining to identify the infarct size. One week after surgery, the rats were randomly assigned into four different groups-MCAO+standard environment (SE), MCAO+enriched environment (EE), Sham+SE and Sham+EE for 4 weeks. At four weeks after MCAO surgery, neurological function deficiency condition and cognitive function were assessed using Longa score and Morris Water Maze prior to euthanasia. The loss or regeneration of myelin was stained with LFB, the expression of myelin regeneration-related protein and microglia protein was quantified by western blot and immunofluorescence, and the level of inflammatory factors was measured by ELISA.EE treatment remarkably decreased the neurological deficit score, ameliorated the cognitive functional deficit in MCAO rats. Furthermore, EE alleviated white matter lesions and demyelination, increased myelin basic protein expression and decreased the number of activated microglia in the hippocampus of MCAO rats. In addition, ELISA analysis indicated that EE decreased the level of IL-1β, IL-6, which further suggests that EE may reduce the level of pro-inflammatory factors by affecting the expression of microglia marker, IBA1, provide a benefit physiological environment for myelin recovery, and improve post stroke cognitive impairment.Our results suggest that exposure to EE substantially reduced the damage to brain tissue caused by activation of microglia activation, decreased the level of pro-inflammatory cytokins, which may induced by microglia, protected and promote white matter recovery to improve cognitive function after stroke. Our findings also indicate exposure to EE is beneficial for patients with white matter impairment characterised by white matter disease-related inflammation.
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