Lotfi Alireza, Abbasi Maryam, Karami Nasrin, Arghavanfar Hadis, Kazeminasab Fatemeh, Rosenkranz Sara K
Department of Exercise Physiology, Ilam Branch, Islamic Azad University, Ilam, Iran.
Department of Exercise Physiology, Ilam Branch, Islamic Azad University, Ilam, Iran.
J Neuroimmunol. 2024 Feb 15;387:578286. doi: 10.1016/j.jneuroim.2024.578286. Epub 2024 Jan 8.
Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS). If demyelination is persistent, it will result in irreversible axonal injury and loss. The purpose of the current study was to investigate the effects of treadmill training on myelin proteomic markers and cerebellum morphology in a rat model of cuprizone-induced toxic demyelination.
Thirty male rats were randomly assigned to five groups (n = 6 per group), consisting of a healthy control group (Control), a cuprizone (CPZ) group, and three exercise training groups: exercise training before and during the CPZ administration (EX-CPZ-EX), exercise training before the CPZ administration (EX-CPZ), and exercise training during the CPZ administration (CPZ-EX). A rat model of CPZ-induced toxic demyelination consisted of feeding the rats cuprizone pellets (0.2%) for 6 weeks. All exercise groups performed a treadmill training protocol 5 days/week for 6 weeks. Levels of Myelin proteolipid protein (PLP), Myelin oligodendrocyte glycoprotein (MOG), axonal injury in the cerebellar tissue, and volume, weight, and length of the cerebellum were determined.
Results indicated a significant decrease in PLP and MOG in the CPZ groups compared to the Control group (****p < 0.0001). There was a significant increase in PLP and MOG and a significant decrease in axonal injury in the EX-CPZ-EX group as compared to other CPZ groups (****p < 0.0001), and CPZ-MS and CPZ-EX were not significantly different from one another. However, there were no significant differences between the groups for the volume, weight, or length of the cerebellum.
Treadmill training improved myelin sheath structural proteins and axonal injury in cerebellar tissue in a rat model of CPZ-induced toxic demyelination.
多发性硬化症（MS）是中枢神经系统（CNS）最常见的脱髓鞘疾病。如果脱髓鞘持续存在，将导致不可逆的轴突损伤和丢失。本研究的目的是探讨跑步机训练对铜螯合剂诱导的毒性脱髓鞘大鼠模型中髓鞘蛋白质组学标志物和小脑形态的影响。
将30只雄性大鼠随机分为五组（每组n = 6），包括健康对照组（Control）、铜螯合剂（CPZ）组和三个运动训练组：在CPZ给药前和给药期间进行运动训练（EX-CPZ-EX）、在CPZ给药前进行运动训练（EX-CPZ）以及在CPZ给药期间进行运动训练（CPZ-EX）。CPZ诱导的毒性脱髓鞘大鼠模型包括给大鼠喂食含0.2%铜螯合剂的颗粒6周。所有运动组每周进行5天的跑步机训练方案，持续6周。测定小脑组织中髓鞘蛋白脂蛋白（PLP）、髓鞘少突胶质细胞糖蛋白（MOG）的水平、轴突损伤以及小脑的体积、重量和长度。
结果表明，与对照组相比，CPZ组的PLP和MOG显著降低（****p < 0.0001）。与其他CPZ组相比，EX-CPZ-EX组的PLP和MOG显著增加，轴突损伤显著降低（****p < 0.0001），并且CPZ-MS和CPZ-EX之间无显著差异。然而，各组之间小脑的体积、重量或长度无显著差异。
在CPZ诱导的毒性脱髓鞘大鼠模型中，跑步机训练改善了小脑组织中的髓鞘结构蛋白和轴突损伤。
