Strength training attenuates neuropathic pain by Preventing dendritic Spine dysgenesis through Suppressing Rac1 and inflammation in experimental autoimmune encephalomyelitis

IF 2.9 3区 医学 Q2 CLINICAL NEUROLOGY Multiple sclerosis and related disorders Pub Date : 2024-11-28 DOI:10.1016/j.msard.2024.106192
Amir Hossein Saffar Kohneh Quchan, Mohammad Reza Kordi, Golrokh Mohammadi, Raheleh Amiri Raeez, Siroos Choobineh
{"title":"Strength training attenuates neuropathic pain by Preventing dendritic Spine dysgenesis through Suppressing Rac1 and inflammation in experimental autoimmune encephalomyelitis","authors":"Amir Hossein Saffar Kohneh Quchan,&nbsp;Mohammad Reza Kordi,&nbsp;Golrokh Mohammadi,&nbsp;Raheleh Amiri Raeez,&nbsp;Siroos Choobineh","doi":"10.1016/j.msard.2024.106192","DOIUrl":null,"url":null,"abstract":"<div><div>Chronic pain is a challenge and major health problem to basic science and clinical practice. Pain is one of the worst symptoms of multiple sclerosis (MS), which has a significant impact on their quality of life. Rac1 is an important intracellular signaling molecule involved in spinal dendritic spine pathology and activation of IL-1β and TNF-α that are associated with chronic neuropathic pain. As a result, targeting Rac1 presents a promising approach to managing neuropathic pain. Clinical studies have demonstrated that physical exercise is a non-pharmacological strategy that positively influences disease progression in individuals with MS, but underlying mechanism of exercise on Rac1- induced neuropathic pain is not well understood. This study examined the effects of a 4-week strength training on Rac1 expression, IL-1B, TNF-α, TGF-β1 levels, MDA concentrations, SOD activity, dendritic spine abnormalities in the dorsal horn of the spinal cord, as well as nociceptive behaviors (formalin test) and motor function (Rotarod test) during the chronic phase of experimental autoimmune encephalomyelitis (EAE). The findings indicated that strength training increased TGF-β1 expression and SOD activity while decreasing the expression of Rac1, IL-1β, TNF-α, and MDA and reducing dendritic spine dysgenesis in the dorsal horn of the spinal cord. We observed strength training effectively reduced nociceptive behaviors and improved motor function in mice with EAE. In summary, regular physical exercise may modulate neuropathic pain through inhibition of dendritic spine dysgenesis, inflammation and oxidative stress in the dorsal horn of the spinal cord.</div></div>","PeriodicalId":18958,"journal":{"name":"Multiple sclerosis and related disorders","volume":"93 ","pages":"Article 106192"},"PeriodicalIF":2.9000,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Multiple sclerosis and related disorders","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2211034824007685","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Chronic pain is a challenge and major health problem to basic science and clinical practice. Pain is one of the worst symptoms of multiple sclerosis (MS), which has a significant impact on their quality of life. Rac1 is an important intracellular signaling molecule involved in spinal dendritic spine pathology and activation of IL-1β and TNF-α that are associated with chronic neuropathic pain. As a result, targeting Rac1 presents a promising approach to managing neuropathic pain. Clinical studies have demonstrated that physical exercise is a non-pharmacological strategy that positively influences disease progression in individuals with MS, but underlying mechanism of exercise on Rac1- induced neuropathic pain is not well understood. This study examined the effects of a 4-week strength training on Rac1 expression, IL-1B, TNF-α, TGF-β1 levels, MDA concentrations, SOD activity, dendritic spine abnormalities in the dorsal horn of the spinal cord, as well as nociceptive behaviors (formalin test) and motor function (Rotarod test) during the chronic phase of experimental autoimmune encephalomyelitis (EAE). The findings indicated that strength training increased TGF-β1 expression and SOD activity while decreasing the expression of Rac1, IL-1β, TNF-α, and MDA and reducing dendritic spine dysgenesis in the dorsal horn of the spinal cord. We observed strength training effectively reduced nociceptive behaviors and improved motor function in mice with EAE. In summary, regular physical exercise may modulate neuropathic pain through inhibition of dendritic spine dysgenesis, inflammation and oxidative stress in the dorsal horn of the spinal cord.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
力量训练通过抑制实验性自身免疫性脑脊髓炎的Rac1和炎症来预防树突状脊柱发育不良,从而减轻神经性疼痛
慢性疼痛是对基础科学和临床实践的挑战和重大健康问题。疼痛是多发性硬化症(MS)最严重的症状之一,严重影响患者的生活质量。Rac1是一个重要的细胞内信号分子,参与脊髓树突棘的病理和IL-1β和TNF-α的激活,这些与慢性神经性疼痛有关。因此,靶向Rac1是治疗神经性疼痛的一种很有前途的方法。临床研究表明,体育锻炼是一种非药物策略,对MS患者的疾病进展有积极影响,但运动对Rac1诱导的神经性疼痛的潜在机制尚不清楚。本研究探讨了4周力量训练对实验性自身免疫性脑脊髓炎(EAE)慢性期大鼠Rac1表达、IL-1B、TNF-α、TGF-β1水平、MDA浓度、SOD活性、脊髓背角树突状棘异常以及伤害性行为(福尔马林试验)和运动功能(Rotarod试验)的影响。结果表明,力量训练增加TGF-β1表达和SOD活性,降低Rac1、IL-1β、TNF-α和MDA表达,减少脊髓背角树突状脊柱发育不良。我们观察到力量训练有效地减少了EAE小鼠的伤害性行为并改善了运动功能。总之,规律的体育锻炼可能通过抑制脊髓背角树突状脊柱发育不良、炎症和氧化应激来调节神经性疼痛。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
5.80
自引率
20.00%
发文量
814
审稿时长
66 days
期刊介绍: Multiple Sclerosis is an area of ever expanding research and escalating publications. Multiple Sclerosis and Related Disorders is a wide ranging international journal supported by key researchers from all neuroscience domains that focus on MS and associated disease of the central nervous system. The primary aim of this new journal is the rapid publication of high quality original research in the field. Important secondary aims will be timely updates and editorials on important scientific and clinical care advances, controversies in the field, and invited opinion articles from current thought leaders on topical issues. One section of the journal will focus on teaching, written to enhance the practice of community and academic neurologists involved in the care of MS patients. Summaries of key articles written for a lay audience will be provided as an on-line resource. A team of four chief editors is supported by leading section editors who will commission and appraise original and review articles concerning: clinical neurology, neuroimaging, neuropathology, neuroepidemiology, therapeutics, genetics / transcriptomics, experimental models, neuroimmunology, biomarkers, neuropsychology, neurorehabilitation, measurement scales, teaching, neuroethics and lay communication.
期刊最新文献
MRI-based radiomics for differention of aquaporin 4-immunoglobulin G–positive neuromyelitis optic spectrum disorder and anti myelin oligodendrocyte glycoprotein immunoglobulin G–associated disorder Impact of oral Cladribine on paramagnetic rim lesions of Multiple Sclerosis patients Women and multiple sclerosis: From gender medicine to precision medicine Ravulizumab and other complement inhibitors for the treatment of autoimmune disorders Walking performance is worse in black than white people with multiple sclerosis
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1