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长期锻炼对实验性自身免疫性脑脊髓炎具有神经保护作用。

Chronic exercise confers neuroprotection in experimental autoimmune encephalomyelitis.

作者信息

Pryor William M, Freeman Kimberly G, Larson Rebecca D, Edwards Gaylen L, White Lesley J

机构信息

Department of Kinesiology, University of Georgia, Athens, Georgia; Department of Neuroscience, The Scripps Research Institute, Jupiter, Florida.

出版信息

J Neurosci Res. 2015 May;93(5):697-706. doi: 10.1002/jnr.23528. Epub 2014 Dec 15.

DOI:10.1002/jnr.23528
PMID:25510644
Abstract

Multiple sclerosis (MS) is an autoimmune disease that affects the CNS, resulting in accumulated loss of cognitive, sensory, and motor function. This study evaluates the neuropathological effects of voluntary exercise in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Two groups of C57BL/6J mice were injected with an emulsion containing myelin oligodendrocyte glycoprotein and then randomized to housing with a running wheel or a locked wheel. Exercising EAE mice exhibited a less severe neurological disease score and later onset of disease compared with sedentary EAE animals. Immune cell infiltration and demyelination in the ventral white matter tracts of the lumbar spinal cord were significantly reduced in the EAE exercise group compared with sedentary EAE animals. Neurofilament immunolabeling in the ventral pyramidal and extrapyramidal motor tracts displayed a more random distribution of axons and an apparent loss of smaller diameter axons, with a greater loss of fluorescence immunolabeling in the sedentary EAE animals. In lamina IX gray matter regions of the lumbar spinal cord, sedentary animals with EAE displayed a greater loss of α-motor neurons compared with EAE animals exposed to exercise. These findings provide evidence that voluntary exercise results in reduced and attenuated disability, reductions in autoimmune cell infiltration, and preservation of axons and motor neurons in the lumbar spinal cord of mice with EAE.

摘要

多发性硬化症(MS)是一种影响中枢神经系统的自身免疫性疾病,会导致认知、感觉和运动功能的累积丧失。本研究评估了自愿运动对实验性自身免疫性脑脊髓炎(EAE)小鼠的神经病理学影响,EAE是MS的一种动物模型。两组C57BL/6J小鼠注射了含有髓鞘少突胶质细胞糖蛋白的乳剂,然后随机分为配备跑步轮或锁定轮的饲养环境。与久坐不动的EAE动物相比,进行运动的EAE小鼠的神经疾病评分较轻,发病时间较晚。与久坐不动的EAE动物相比,EAE运动组小鼠腰脊髓腹侧白质束中的免疫细胞浸润和脱髓鞘明显减少。腹侧锥体和锥体外运动束中的神经丝免疫标记显示轴突分布更随机,小直径轴突明显丢失,久坐不动的EAE动物的荧光免疫标记丢失更多。在腰脊髓的IX层灰质区域,与进行运动的EAE动物相比,久坐不动的EAE动物的α运动神经元损失更大。这些发现提供了证据,表明自愿运动可减少和减轻EAE小鼠的残疾程度,减少自身免疫细胞浸润,并保护腰脊髓中的轴突和运动神经元。

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