Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats.

IF 4.7 2区 心理学 Q1 BEHAVIORAL SCIENCES
Dina M Monir, Motamed E Mahmoud, Omyma G Ahmed, Ibrahim F Rehan, Amany Abdelrahman
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引用次数: 8

Abstract

Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions, and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism. This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of the Nrf2- ARE pathway as a mechanism involved in exercise-associated improvement in rotenone-induced PD in rats.

Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination)groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.

Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone-induced PD. When treadmill exercise was introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor coordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to Nrf2 pathways such as TFAM, Nrf2 and NQO.1 mRNA expression.

Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating the Nrf2 pathway.

Abstract Image

Abstract Image

Abstract Image

在鱼藤酮治疗的大鼠中,强迫运动激活纹状体中的NrF2通路,改善帕金森病的运动和行为表现。
背景:帕金森病(PD)是一种常见的神经退行性疾病,其特征是黑质纹状体多巴胺能神经元的进行性丧失,导致多巴胺消耗和运动、情绪和认知问题。虽然PD的发病机制尚不清楚,但氧源性自由基对多巴胺能神经元的损伤被认为是一个重要的机制。本研究旨在评估跑步机运动在雄性Wister大鼠中作为单一治疗和左旋多巴辅助治疗鱼藤酮诱导的PD的作用。研究Nrf2- ARE通路在鱼藤酮诱导的大鼠帕金森病运动相关改善中的作用。方法:将动物分为5组,分别为对照组、鱼藤酮组、鱼藤酮\运动组、鱼藤酮\左旋多巴组和鱼藤酮\运动\左旋多巴(联合)组。PD诱导后,鱼藤酮运动组和联合组大鼠每天在跑步机上运动4周。结果:跑步机运动显著改善鱼藤酮诱导PD的行为和运动方面。当跑步机运动作为单一干预引入时,它改善了PD的大多数行为方面,步态完全纠正,短期记忆和运动协调。左旋多巴纠正了运动活动和运动协调,但未能改善短期记忆,仅部分纠正鱼藤酮治疗大鼠的步态。当跑步机运动与左旋多巴联合使用时,PD的所有特征都得到了纠正。结果发现,运动上调了部分与Nrf2通路相关的基因,如TFAM、Nrf2和nq01 mRNA的表达。结论:本研究表明,强迫运动通过激活Nrf2通路改善帕金森样特征。
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来源期刊
Behavioral and Brain Functions
Behavioral and Brain Functions 医学-行为科学
CiteScore
5.90
自引率
0.00%
发文量
11
审稿时长
6-12 weeks
期刊介绍: A well-established journal in the field of behavioral and cognitive neuroscience, Behavioral and Brain Functions welcomes manuscripts which provide insight into the neurobiological mechanisms underlying behavior and brain function, or dysfunction. The journal gives priority to manuscripts that combine both neurobiology and behavior in a non-clinical manner.
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