补充NAD+可以缓解慢性睡眠限制 (CSR) 诱导的微质前炎症 in vivo和 in vitro
Qiqiang Chen1, Jinrong Xiao1, Zhenya Lin1
1Department of Anesthesiology, The 900 Hospital of the Joint Logistic Support Force of the People's Liberation Army of China, Fuzhou 350025, China.
Journal of neuroimmunology
|November 9, 2024
概括
尼古丁胺胺氨基二核酸 (NAD+) 补充剂减轻了由慢性睡眠限制引起的认知衰退和神经炎症. 通过减少氧化应激和调节cGAS-STING/NF-κB通路,NAD+保护微质,为睡眠相关的神经问题提供了有前途的治疗方法.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 睡眠不足是一个全球性的健康问题,与神经发育障碍和认知障碍有关.
- 中枢神经系统 (CNS) 中的主要免疫细胞微质细胞在睡眠剥夺引起的神经损伤中至关重要.
- 尼古丁胺胺氨基二核酸 (NAD+) 是一种重要的辅酶,在微质中具有抗炎和线粒体保护性质,但其在睡眠剥夺中的作用尚不清楚.
研究的目的:
- 研究NAD+对慢性睡眠限制 (CSR) 诱导的神经系统缺陷的神经保护作用.
- 阐明NAD+作用的潜在机制,重点关注微质功能和炎症通路.
主要方法:
- 建立了体内和体外模型来模拟慢性睡眠限制.
- 利用行为测试和免疫光染色来评估认知功能和微质激活.
- 进行生物化学测试以分析氧化应激,线粒体功能和炎症信号通路 (cGAS-STING/NF-κB).
主要成果:
- 在CSR模型中,NAD+补充显著改善了认知衰退,并减少了微质激活.
- NAD+治疗降低了促炎性细胞因子表达,氧化应激和微质中的线粒体损伤.
- 在体外研究证实了NAD+抑制的活性氧物种 (ROS) 生产和调节的微质极化 (M1到M2).
- NAD+的给药降低了激活的cGAS-STING/NF-κB通路的调节,而STING对抗作用部分验证了这一机制.
结论:
- 补充NAD+证明了对慢性睡眠限制引起的神经问题的显著神经保护潜力.
- NAD+通过调节微质炎症反应,减少氧化应激,并影响cGAS-STING通路来发挥其作用.
- 该cGAS-STING通路被确定为睡眠剥夺引起的微质炎症的关键调节器,这表明NAD+是一种可行的治疗策略.
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