Neuroprotective effect of long-term resistance physical exercise against memory damage elicited by a lipopolysaccharide-induced neuroinflammation model in male rats

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Vanessa Valéria Miron, Charles Elias Assmann, Vitor Bastianello Mostardeiro, Marcylene Vieira da Silveira, Priscila Marquezan Copetti, Bianca Fagan Bissacotti, Adriel Antonio Schirmann, Milagros Fanny Vera Castro, Jessié Martins Gutierres, Marilda da Cruz Fernandes, Fernanda Tibolla Viero, Vera Maria Morsch, Maria Rosa Chitolina Schetinger, Andréia Machado Cardoso
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Abstract

Resistance exercise training (RET) is considered an excellent tool for preventing diseases with an inflammatory background. Its neuroprotective, antioxidant, and anti-inflammatory properties are responsible for positively modulating cholinergic and oxidative systems, promoting neurogenesis, and improving memory. However, the mechanisms behind these actions are largely unknown. In order to investigate the pathways related to these effects of exercise, we conducted a 12-week long-term exercise training protocol and used lipopolysaccharide (LPS) to induce damage to the cortex and hippocampus of male Wistar rats. The cholinergic system, oxidative stress, and histochemical parameters were analyzed in the cerebral cortex and hippocampus, and memory tests were also performed. It was observed that LPS: (1) caused memory loss in the novel object recognition (NOR) test; (2) increased the activity of acetylcholinesterase (AChE) and Iba1 protein density; (3) reduced the protein density of brain-derived neurotrophic factor (BDNF) and muscarinic acetylcholine receptor M1 (CHRM1); (4) elevated the levels of lipid peroxidation (TBARS) and reactive species (RS); and (5) caused inflammatory damage to the dentate gyrus. RET, on the other hand, was able to prevent all alterations induced by LPS, as well as increase per se the protein density of the alpha-7 nicotinic acetylcholine receptor (nAChRα7) and Nestin, and the levels of protein thiols (T-SH). Overall, our study elucidates some mechanisms that support resistance physical exercise as a valuable approach against LPS-induced neuroinflammation and memory loss.

长期阻力运动对脂多糖诱导的雄性大鼠神经炎症模型引起的记忆损伤的神经保护作用
阻力运动训练(RET)被认为是预防炎症性疾病的绝佳工具。它具有神经保护、抗氧化和抗炎特性,能积极调节胆碱能和氧化系统,促进神经发生,改善记忆。然而,这些作用背后的机制在很大程度上是未知的。为了研究与运动的这些作用相关的途径,我们进行了为期 12 周的长期运动训练方案,并使用脂多糖(LPS)诱导雄性 Wistar 大鼠的大脑皮层和海马受损。对大脑皮层和海马的胆碱能系统、氧化应激和组织化学参数进行了分析,并进行了记忆测试。结果表明,LPS(1)导致新物体识别(NOR)测试中的记忆丧失;(2)增加乙酰胆碱酯酶(AChE)的活性和 Iba1 蛋白密度;(3)降低脑源性神经营养因子(BDNF)和毒蕈碱乙酰胆碱受体 M1(CHRM1)的蛋白密度;(4)升高脂质过氧化物(TBARS)和活性物质(RS)的水平;(5)导致齿状回炎症性损伤。而 RET 则能防止 LPS 引起的所有变化,并能增加α-7 尼古丁乙酰胆碱受体(nAChRα7)和 Nestin 的蛋白质密度以及蛋白质硫醇(T-SH)的水平。总之,我们的研究阐明了一些机制,这些机制支持将抗阻力体育锻炼作为一种有价值的方法来对抗 LPS 诱导的神经炎症和记忆力减退。
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来源期刊
Journal of Neuroscience Research
Journal of Neuroscience Research 医学-神经科学
CiteScore
9.50
自引率
2.40%
发文量
145
审稿时长
1 months
期刊介绍: The Journal of Neuroscience Research (JNR) publishes novel research results that will advance our understanding of the development, function and pathophysiology of the nervous system, using molecular, cellular, systems, and translational approaches. JNR covers both basic research and clinical aspects of neurology, neuropathology, psychiatry or psychology. The journal focuses on uncovering the intricacies of brain structure and function. Research published in JNR covers all species from invertebrates to humans, and the reports inform the readers about the function and organization of the nervous system, with emphasis on how disease modifies the function and organization.
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