PubMed日本語 - β-amyloid₁₋₄₀ペプチドによって誘発されるアルツハイマー病のマウス・モデルの運動の神経保護の効果。―QLifePro医療翻訳医療翻訳 QLifePro


Neuroprotective effect of physical exercise in a mouse model of Alzheimer's disease induced by β-amyloid₁₋₄₀ peptide.


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Leandro C Souza, Carlos B Filho, André T R Goes, Lucian Del Fabbro, Marcelo G de Gomes, Lucielli Savegnago, Mauro Schneider Oliveira, Cristiano R Jesse


Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas-LaftamBio Pampa, Universidade Federal do Pampa, Itaqui, RS, CEP 97650-000, Brazil.


This study was designed to investigate the potential neuroprotective effect of exercise in a mouse model of Alzheimer's disease (AD) induced by intracerebroventricular (i.c.v.) injection of beta-amyloid₁₋₄₀ (Aβ₁₋₄₀) peptide. For this aim, male Swiss Albino mice were submitted to swimming training (ST) with progressive increase in intensity and duration for 8 weeks before Aβ₁₋₄₀ administration (400 pmol/animal; 3 μl/site, i.c.v. route). The cognitive behavioral, oxidative stress, and neuroinflammatory markers in hippocampus and prefrontal cortex of mice were assessed 7 days after Aβ₁₋₄₀ administration. Our results demonstrated that ST was effective in preventing impairment in short- and long-term memories in the object recognition test. ST attenuated the increased levels of reactive species and decreased non-protein thiol levels in hippocampus and prefrontal cortex induced by Aβ₁₋₄₀. Also, Aβ₁₋₄₀ inhibited superoxide dismutase activity and increased glutathione peroxidase, glutathione reductase, and glutathione S-transferase activities in hippocampus and prefrontal cortex-alterations that were mitigated by ST. In addition, ST was effective against the increase of tumor necrosis factor-alpha and interleukin-1 beta levels and the decrease of interleukin-10 levels in hippocampus and prefrontal cortex. This study confirmed the hypothesis that exercise is able to protect against some mechanisms of Aβ₁₋₄₀-induced neurotoxicity. In conclusion, we suggest that exercise can prevent the cognitive decline, oxidative stress, and neuroinflammation induced by Aβ₁₋₄₀ in mice supporting the hypothesis that exercise can be used as a non-pharmacological tool to reduce the symptoms of AD.


この目的のために、雄のスイスの白子のマウスは、Aβ₁₋₄₀当局(400pmol/動物; 3μl/部位、i.c.v.ルート)の前に、8週の間強度と期間の漸進性増加で、水泳訓練(ST)に提出された。

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