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

中文翻译：

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强迫运动激活纹状体中的 NrF2 通路，改善鱼藤酮治疗大鼠帕金森病的运动和行为表现

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进行性丧失，导致多巴胺耗竭以及运动、情绪和认知问题。虽然帕金森病的发病机制尚不清楚，但氧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对鱼藤酮诱导的 PD 的作用。研究 Nrf2-ARE 通路作为参与运动相关改善鱼藤酮诱导的大鼠帕金森病的机制的作用。将动物分为5组（对照、鱼藤酮、鱼藤酮\运动、鱼藤酮\L-多巴和鱼藤酮\运动\L-多巴（组合）组）。PD诱导后，鱼藤酮\运动组和联合组的大鼠每天在跑步机上运动，持续4周。跑步机锻炼显着改善了鱼藤酮引起的帕金森病的行为和运动方面。当跑步机运动作为单一干预措施引入时，它改善了 PD 的大多数行为方面，完全纠正步态、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，并且仅部分纠正了鱼藤酮治疗大鼠的步态。当跑步机运动与左旋多巴相结合时，PD 的所有特征均得到纠正。研究发现，运动上调了一些与 Nrf2 通路相关的基因，例如 TFAM、Nrf2 和 NQO.1 mRNA 表达。这项研究表明，强迫运动通过激活 Nrf2 通路来改善帕金森病样特征。