Swimming Exercise Ameliorates Symptoms of MOG-Induced Experimental Autoimmune Encephalomyelitis by Inhibiting Inflammation and Demyelination in Rats

International Neurourology Journal

Eun-Surk Yi¹  Ji-Youn Kim¹  Hyunju Lee²  Sung-Eun Kim³  Chang-Ju Kim³  Il-Gyu Ko³  Jun-Su Kim⁴  Yong-Seok Jee⁵ 

[1] Department of Exercise Rehabilitation & Welfare, Gachon University, Incheon, Korea;Department of Health Administration, College of Medical Health, Jungwon University, Goesan, Korea;Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea;Department of Sports & Outdoors, College of Health Industry, Eulji University, Seongnam, Korea;Research Institute of Sports and Industry Science, Hanseo University, Seosan, Korea;

关键词: multiple sclerosis;    experimental autoimmune encephalomyelitis;    swimming exercise;    inflammation;    demyelination;   

DOI  :  10.5213/inj.2040156.078

来源: DOAJ

【 摘 要 】

Purpose Multiple sclerosis is an autoimmune disease that affects the central nerve system, resulting in cumulative loss of motor function. Multiple sclerosis is induced through multiple mechanisms and is caused by inflammation and demyelination. This study aims to evaluate the neuroprotective effect of swimming exercise in experimental autoimmune encephalomyelitis (EAE) rats, an animal model of multiple sclerosis. Methods EAE was induced by an intradermal injection of 50-μg purified myelin oligodendrocyte glycoprotein 33–55 (MOG33-55) dissolved in 200-μL saline at the base of the tail. The rats in the swimming exercise group were made to swim for 30 minutes once pert a day for 26 consecutive days, starting 5 days after induction of EAE. To compare the effect of swimming exercise with interferon-β, a drug for multiple sclerosis, interferon-β was injected intraperitoneally into rats of the EAE-induced and interferon-β-treated group during the exercise period. Results Injection of MOG33-55 caused weight loss, decreased clinical disability score, and increased level of pro-inflammatory cytokines and inflammatory mediators in the lumbar spinal cord. Loss of motor function and weakness increased demyelination score. Swimming exercise suppressed demyelination and expression of pro-inflammatory cytokines and inflammatory mediators. These changes promoted recovery of EAE symptoms such as body weight loss, motor dysfunction, and weakness. Swimming exercise caused the same level of improvement as interferon-β treatment. Conclusions The results of this experiment suggest the possibility of swimming exercise in urological diseases that are difficult to treat. Swimming exercises can be considered for relief of symptom in incurable multiple sclerosis.

【 授权许可】

Unknown