褪黑素通过核因子κ b通路和氧化应激影响急性睡眠剥夺小鼠认知功能障碍的作用。

IF 2.2 4区 医学 Q4 NEUROSCIENCES
Translational Neuroscience Pub Date : 2025-10-07 eCollection Date: 2025-01-01 DOI:10.1515/tnsci-2025-0379
Wenting Li, Quan Chen, Haipeng Fu
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引用次数: 0

摘要

目的:急性睡眠剥夺(ASD)在当代社会普遍存在。本研究通过核因子κ b (NF-κB)通路和氧化应激机制探讨褪黑素对ASD小鼠认知功能障碍(CD)的影响机制。方法:建立ASD小鼠模型,分别给予低剂量和高剂量褪黑素、NF-κB抑制剂PDTC或脂多糖(LPS)治疗,评估其空间记忆、自发活动和焦虑水平。HE染色、尼氏染色观察海马形态及神经元状态。海马CA1区突触后密度蛋白95 (PSD95)、磷酸化(p)-p65和p- i - κ b蛋白的活性和水平;乙酰胆碱酯酶(AChE)、乙酰胆碱(ACh)、丙二醛(MDA)和活性氧(ROS);采用western blot和ELISA试剂盒检测IL-4、IL-10、肿瘤坏死因子(TNF) -α、IL-1β水平。结果:ASD小鼠表现为学习记忆能力和自发活动减弱,海马CA1区细胞排列松散,细胞体边界不清,间隙增大,神经元损伤严重,PSD95蛋白水平降低。ASD小鼠海马CA1区AChE、p-p65、p- i - κ b、TNF-α、IL-1β、MDA、ROS水平升高,ACh、IL-4、IL-10水平降低,SOD活性降低。褪黑素或PDTC抑制了NF-κB通路,下调了ASD小鼠海马CA1区TNF-α、IL-1β、MDA、ROS活性,上调了IL-4、IL-10和SOD活性,提高了学习记忆能力。lps诱导的NF-κB通路激活部分避免了褪黑素对ASD小鼠的有益作用。结论:褪黑素通过调节NF-κB通路和氧化应激改善asd诱导的小鼠CD。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of melatonin in affecting cognitive dysfunction in acute sleep deprivation mice through the nuclear factor kappaB pathway and oxidative stress.

Objective: Acute sleep deprivation (ASD) is prevalent in contemporary society. This study explored the mechanism of melatonin affecting cognitive dysfunction (CD) in ASD mice through the nuclear factor kappaB (NF-κB) pathway and oxidative stress.

Methods: The ASD mouse model was established and treated with low-dose and high-dose melatonin, a NF-κB inhibitor PDTC, or lipopolysaccharide (LPS), with their spatial memory, spontaneous activity, and anxiety assessed. Hippocampal morphology and neuronal status were observed via HE and Nissl staining. Superoxide dismutase (SOD) activity and levels of hippocampal CA1 region postsynaptic density protein 95 (PSD95), phosphorylated (p)-p65, and p-IκB proteins; acetylcholinesterase (AChE), acetylcholine (ACh), malondialdehyde (MDA), and reactive oxygen species (ROS); and IL-4, IL-10, tumor necrosis factor [TNF]-α, and IL-1β levels were determined by western blot and ELISA kits.

Results: ASD mice exhibited reduced learning and memory abilities and spontaneous activities, loosely-arranged cells in the hippocampal CA1 region, unclear cell body boundaries, enlarged gaps, severe neuronal damage, and reduced PSD95 protein level. There were increases in AChE, p-p65, p-IκB, TNF-α, IL-1β, MDA, and ROS levels, decrements in ACh, IL-4, and IL-10 levels and SOD activity in the hippocampal CA1 region of ASD mice. Melatonin or PDTC inhibited the NF-κB pathway, down-regulated TNF-α, IL-1β, MDA, and ROS and up-regulated IL-4 and IL-10 and SOD activity in the hippocampal CA1 region of ASD mice, and improved the learning and memory abilities. LPS-induced NF-κB pathway activation partially averted melatonin's beneficial effects on ASD mice.

Conclusion: Melatonin ameliorated ASD-induced CD in mice by modulating the NF-κB pathway and oxidative stress.

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来源期刊
CiteScore
3.00
自引率
4.80%
发文量
45
审稿时长
>12 weeks
期刊介绍: Translational Neuroscience provides a closer interaction between basic and clinical neuroscientists to expand understanding of brain structure, function and disease, and translate this knowledge into clinical applications and novel therapies of nervous system disorders.
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