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通过PI3K/AKT/mTOR途径促进微细胞自,VCPIP1可改善与败血症相关的脑病变

Jing Zuo¹, Ruiwen Ding¹, Xing Wang¹

¹The Research Centre of Anesthesiology and Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, Wuchang, 169 Donghu Road, Hubei Province, China.

International immunopharmacology

|August 27, 2025

概括

微质中含有瓦洛的蛋白相互作用蛋白1 (VCPIP1) 在败血症相关脑病 (SAE) 期间调节大脑功能. 抑制VCPIP1增强微细胞自,减少SAE中的神经炎症和认知缺陷.

科学领域:

神经科学
免疫学
分子生物学

背景情况:

败血症相关脑病变 (SAE) 是系统性感染的严重神经并发症.
微质在SAE的发病过程中起着至关重要的作用.
含有瓦洛辛的蛋白相互作用蛋白1 (VCPIP1) 在微质中高度表达,并与神经炎症有关.

研究的目的:

在SAE期间调查VCPIP1在微质中的作用.
阐明VCPIP1在SAE发病过程中的潜在分子机制.
探索VCPIP1作为SAE的潜在治疗点.

主要方法:

人类蛋白质图谱和单细胞RNA测序数据的生物信息学分析.
为SAE建立小鼠结和穿孔 (CLP) 模型
在野生型和VCPIP1缺乏的小鼠中评估学习和记忆,微细胞自,细胞因子产生和信号通路激活 (PI3K/AKT/mTOR).
使用LY294002进行PI3K的药理抑制.

主要成果:

在SAE小鼠模型中,VCPIP1在海马微细胞上升调节.
在SAE中,VCPIP1缺乏会加剧认知障碍,抑制微细胞自,并增加促炎细胞因子的产生.
缺少VCPIP1会激活PI3K/AKT/mTOR通路,从而抑制自流.
用LY294002抑制PI3K恢复了自,减少了神经炎症,并减轻了神经元损伤.

结论:

在SAE中,VCPIP1通过抑制PI3K/ AKT/ mTOR途径促进微细胞自.
在SAE中,VCPIP1缺乏导致自功能受损和神经炎症加剧.
在SAE中,VCPIP1是缓解神经炎症和认知功能障碍的有希望的治疗点.

关键词:

自食神经炎症与败血症相关的脑病变在VCPIP1

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PI3K/mTOR/AKT Signaling Pathway

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