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Swimming and strength exercise improve clinical abnormalities of mice with experimental autoimmune encephalomyelitis by modulating key neuroimmunological pathways

In: Comparative Exercise Physiology
Authors:
S.E. Andani Department of Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran

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https://orcid.org/0000-0002-1300-6757
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S. Shahrbanian Department of Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran

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https://orcid.org/0000-0003-3104-7584
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M.R. Kordi Department of Exercise Physiology, Faculty of Sport and Health Sciences, University of Tehran, Tehran, Iran

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https://orcid.org/0000-0002-6507-6634
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M.M. Shamsi Department of Physical Education and Sport Sciences, Yazd University, Yazd, Iran
Department of Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran

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https://orcid.org/0000-0003-4665-5363
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Abstract

Experimental autoimmune encephalomyelitis (EAE) affects the Ido1-Ahr-Odc1 signaling axis, which has been identified as a potential treatment endpoint in EAE. This study aimed to compare the effects of different exercise regimens on this axis in the cerebellum of EAE mice. Forty mice were divided into four groups: (1) healthy controls, (2) mice with EAE, (3) EAE mice treated with swimming exercise, and (4) EAE mice treated with strength exercise. Mice were subjected to two distinct exercise interventions for 30 min/day, 5 days/week, over 4 weeks. Quantitative gene expression analysis of indoleamine 2, 3-dioxygenase 1 (Ido1), aryl hydrocarbon receptor (Ahr), ornithine decarboxylase 1 (Odc1), spermidine synthetase (Spds), and arylalkylamine N-acetyltransferase (Aanat) was performed using RT-PCR. Clinical signs and body weight were recorded daily in all mice. Motor performance was evaluated using the rotarod test. Results showed significant changes in the expression of Ido1 (F = 77.08, P = < 0.001), Ahr (F = 225.95, P = < 0.001), Odc1 (F = 116.27, P = < 0.001), Spds (F = 67.796, P = < 0.001), Aanat ( P < 0.001, F = 84.72). Both swimming and strength exercises significantly downregulated the expression of Ido1, Ahr, Odc1, and Spds compared with the EAE control group ( P < 0.001). Expression of the Aanat gene decreased, although this difference was not statistically significant ( P = 0.438). Clinical scores, body weight, and motor performance improved in all exercise groups ( P < 0.01). EAE progression may be attenuated by swimming and strength exercise, primarily by inducing suppression of gene expression along the axis of Ido1-Ahr-Oc1.

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