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游泳训练可改善 ALS 小鼠的过度活跃,并增加脊髓中的谷胱甘肽过氧化物酶活性。

Swim Training Ameliorates Hyperlocomotion of ALS Mice and Increases Glutathione Peroxidase Activity in the Spinal Cord.

机构信息

Department of Animal and Human Physiology, Faculty of Biology, University of Gdansk, 80-309 Gdansk, Poland.

Department of Pharmaceutical Pathophysiology, Faculty of Pharmacy, Medical University of Gdansk, 80-211 Gdansk, Poland.

出版信息

Int J Mol Sci. 2021 Oct 27;22(21):11614. doi: 10.3390/ijms222111614.

DOI:10.3390/ijms222111614
PMID:34769048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8583724/
Abstract

(1) Background: Amyotrophic lateral sclerosis (ALS) is an incurable, neurodegenerative disease. In some cases, ALS causes behavioral disturbances and cognitive dysfunction. Swimming has revealed a neuroprotective influence on the motor neurons in ALS. (2) Methods: In the present study, a SOD1-G93A mice model of ALS were used, with wild-type B6SJL mice as controls. ALS mice were analyzed before ALS onset (10th week of life), at ALS 1 onset (first symptoms of the disease, ALS 1 onset, and ALS 1 onset SWIM), and at terminal ALS (last stage of the disease, ALS TER, and ALS TER SWIM), and compared with wild-type mice. Swim training was applied 5 times per week for 30 min. All mice underwent behavioral tests. The spinal cord was analyzed for the enzyme activities and oxidative stress markers. (3) Results: Pre-symptomatic ALS mice showed increased locomotor activity versus control mice; the swim training reduced these symptoms. The metabolic changes in the spinal cord were present at the pre-symptomatic stage of the disease with a shift towards glycolytic processes at the terminal stage of ALS. Swim training caused an adaptation, resulting in higher glutathione peroxidase (GPx) and protection against oxidative stress. (4) Conclusion: Therapeutic aquatic activity might slow down the progression of ALS.

摘要

(1) 背景:肌萎缩侧索硬化症(ALS)是一种无法治愈的神经退行性疾病。在某些情况下,ALS 会导致行为障碍和认知功能障碍。游泳对 ALS 中的运动神经元具有神经保护作用。(2) 方法:本研究使用 SOD1-G93A 型 ALS 小鼠模型,以野生型 B6SJL 小鼠作为对照。在 ALS 发病前(第 10 周)、ALS 发病时(疾病的第一个症状,ALS 发病时和 ALS 发病时游泳)和终末期 ALS(疾病的最后阶段,ALS TER 和 ALS TER 游泳)时对 ALS 小鼠进行分析,并与野生型小鼠进行比较。游泳训练每周进行 5 次,每次 30 分钟。所有小鼠均进行行为测试。对脊髓进行酶活性和氧化应激标志物分析。(3) 结果:无症状 ALS 小鼠的运动活性高于对照小鼠;游泳训练减轻了这些症状。疾病的无症状阶段出现了脊髓代谢变化,在 ALS 的终末期,糖酵解过程发生了转变。游泳训练引起了适应,导致谷胱甘肽过氧化物酶(GPx)升高和氧化应激的保护作用。(4) 结论:治疗性水上活动可能会减缓 ALS 的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/344854ac056c/ijms-22-11614-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/344854ac056c/ijms-22-11614-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/effe2ba7722d/ijms-22-11614-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/87b64e7a4128/ijms-22-11614-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/2e87270c1e9d/ijms-22-11614-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/eb25c5db3535/ijms-22-11614-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49e4/8583724/344854ac056c/ijms-22-11614-g007.jpg

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