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比较性海马体转录组学揭示了在败血症相关脑病变中模型特定的途径和融合性炎症

Xueling Zhang¹, Mengshi Yang¹, Yaxuan Zhang¹

¹Department of Intensive Care Unit, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Neuromolecular medicine

|November 27, 2025

概括

败血症相关脑病变 (SAE) 模型显示出明显的海马基因表达. CLP和LPS模型显示神经炎症,而PCI模型显示代谢变化,关键的基因和途径得到验证.

科学领域:

神经科学是一个神经科学.
基因组学就是基因组学.
免疫学免疫学免疫学

背景情况:

败血症相关脑病变 (SAE) 是败血症的严重并发症,死亡率高.
现有的动物模型 (CLP,LPS,PCI) 诱导各种炎症反应和海马的影响.

研究的目的:

在不同的SAE动物模型中全面比较海马体的转录基因特征.
识别和验证SAE的核心分子特征.

主要方法:

公开的转录基因数据集的生物信息分析 (GSE253309,GSE226120,GSE167610).
重量基因同表达网络分析 (WGCNA) 和蛋白与蛋白相互作用 (PPI) 网络构建.
使用CLP诱导的SAE小鼠模型和海马RNA测序的独立验证.

主要成果:

临床皮肤炎和临床皮肤炎模型共享神经炎症特征 (免疫/炎症反应,TNF,NF-κB,IL-17通路).
PCI模型显示了与细胞迁移和代谢途径 (胆汁分泌,甲酸盐/阿尔达酸盐代谢) 相关的独特特征.
独立验证证实了CLP模型发现的强烈一致性,验证了关键基因 (Lcn2,S100a8,S100a9,Lrg1) 和途径.

结论:

CLP和LPS模型表现出与PCI模型不同的合性海马体转录组概况.
特定的基因 (Lcn2,S100a8,S100a9,Lrg1) 和信号通路 (TNF,IL-17) 是SAE的可靠核心特征.

关键词:

切卡结合和穿孔的情况.脂聚糖类糖化物脂聚糖类糖化物腹膜污染和感染败血症相关的脑病变 - - 败血症相关的脑病变信号通道的信号路径.转录组转录组就是一个转录组.

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