Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas, LaftamBio Pampa, Universidade Federal do Pampa, CEP 97650-000 Itaqui, RS, Brazil.
Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas, LaftamBio Pampa, Universidade Federal do Pampa, CEP 97650-000 Itaqui, RS, Brazil.
Neuroscience. 2014 Jan 3;256:61-71. doi: 10.1016/j.neuroscience.2013.09.042. Epub 2013 Oct 1.
Parkinson's disease (PD) is characterized by progressive dopamine (DA) depletion in the striatum. Exercise has been shown to be a promising non-pharmacological approach to reduce the risk of neurodegeneration diseases. This study was designed to investigate the potential neuroprotective effect of swimming training (ST) in a mouse model of PD induced by 6-hydroxydopamine (6-OHDA) in mice. The present study demonstrated that a 4-week ST was effective in attenuating the following impairments resulting from 6-OHDA exposure: (i) depressive-like behavior in the tail suspension test; (ii) increase in the number of falls in the rotarod test; (iii) impairment on long-term memory in the object recognition test; (iv) increase of the reactive species and interleukin 1-beta (IL-1β) levels; (v) inhibition of the glutathione peroxidase (GPx) activity; (vi) rise of the glutathione reductase (GR) and glutathione S-transferase (GST) activities and vii) decrease of DA, homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) levels. The mechanisms involved in this study are the modulation of GPx, GR and GST activities as well as IL-1β level in a PD model induced by 6-OHDA, protecting against the decrease of DA, DOPAC and HVA levels in the striatum of mice. These findings reinforce that one of the effects induced by exercise on neurodegenerative disease, such as PD, is due to antioxidant and anti-inflammatory properties. We suggest that exercise attenuates cognitive and motor declines, depression, oxidative stress, and neuroinflammation induced by 6-OHDA supporting the hypothesis that exercise can be used as a non-pharmacological tool to reduce the symptoms of PD.
帕金森病（PD）的特征是纹状体中多巴胺（DA）的进行性耗竭。运动已被证明是一种有前途的非药物方法，可以降低神经退行性疾病的风险。本研究旨在研究游泳训练（ST）在 6-羟多巴胺（6-OHDA）诱导的 PD 小鼠模型中的潜在神经保护作用。本研究表明，4 周的 ST 有效减轻了 6-OHDA 暴露引起的以下损伤：（i）在悬尾试验中出现的抑郁样行为；（ii）在转棒试验中跌倒次数增加；（iii）在物体识别试验中出现的长期记忆障碍；（iv）活性物质和白细胞介素 1-β（IL-1β）水平增加；（v）谷胱甘肽过氧化物酶（GPx）活性抑制；（vi）谷胱甘肽还原酶（GR）和谷胱甘肽 S-转移酶（GST）活性升高；（vii）DA、高香草酸（HVA）和 3,4-二羟基苯乙酸（DOPAC）水平降低。本研究涉及的机制是调节 GPx、GR 和 GST 活性以及 IL-1β水平在 6-OHDA 诱导的 PD 模型中，防止小鼠纹状体中 DA、DOPAC 和 HVA 水平下降。这些发现强化了运动对神经退行性疾病（如 PD）的一种影响是由于抗氧化和抗炎特性。我们建议运动减轻由 6-OHDA 引起的认知和运动能力下降、抑郁、氧化应激和神经炎症，支持运动可以用作减轻 PD 症状的非药物工具的假说。
