有氧运动通过减少氧化应激,质激活和神经炎症来减轻LPS诱导的认知功能障碍
Jae-Won Choi1, Sang-Woo Jo2, Dae-Eun Kim1
1Department of Physical Education, Yonsei University, Seoul, 03722, South Korea.
Redox biology
|February 26, 2024
概括
有氧运动通过减少神经炎症来改善小鼠的记忆和认知功能. 这可以通过增加FNDC5 / 虹膜蛋白的表达来实现,它可以激活神经保护通路并抑制大脑中的炎症反应.
科学领域:
- 神经科学是一个神经科学.
- 运动生理学 运动生理学
- 免疫学 免疫学 免疫学
背景情况:
- 衰老与认知能力下降和记忆障碍有关.
- 身体活动,特别是有氧运动,在缓解与年龄相关的认知缺陷方面表现有前途.
- 通过有氧运动发挥神经保护作用的精确机制仍然不完全理解.
研究的目的:
- 为了研究有氧运动的神经保护和抗炎作用,在由脂多糖 (LPS) 诱导的记忆丧失的小鼠模型中.
- 探索FNDC5/伊利辛在调解有氧运动对LPS诱导的神经炎症的益处中的作用.
- 检查有氧运动对微质激活和相关炎症通路的影响.
主要方法:
- 在体内:C57BL/6J小鼠接受了为期4周的有氧运动训练,并每周注射LPS.
- 在体外:用LPS刺激BV-2微质细胞,然后用虹素治疗.
- 测量包括认知功能的行为测试,蛋白质表达分析 (FNDC5,BDNF,CREB,Nrf2/HO-1,BACE-1,iNOS,COX-2),以及对炎症信号通路 (NF-κB,MAPK,IRF3) 的评估.
主要成果:
- 在接受LPS治疗的小鼠中,有氧运动显著改善了记忆障碍和认知缺陷.
- 运动增加了FNDC5,BDNF,CREB,Nrf2和HO-1的表达,同时减少了海马和大脑皮层中的BACE-1表达.
- 在体外,虹膜素治疗抑制了LPS诱导的NF-κB,MAPK和IRF3信号的激活,减少了iNOS和COX-2,并在微质细胞中增强了Nrf2/HO-1表达.
结论:
- 有氧运动增强了LPS诱导的记忆丧失小鼠的空间学习和认知功能.
- 这些益处通过通过FNDC5 / 伊利辛通路抑制微质介导的神经炎症来调节.
- 有氧运动促进神经保护,并通过BDNF/FNDC5/素轴减少炎症.
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