抑制FKBP5缓解炎症和肠道屏障功能障碍在败血症
Jian Li1, Anwaier Apizi1, Tingting Song1
1Department of Critical Care Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi, People's Republic of China.
概括
抑制FK506结合蛋白5 (FKBP5) 通过减少炎症和屏障功能障碍,保护免受败血症引起的肠损伤. 这部分是通过抑制核因子kappa B (NF-κB) 信号通路来实现的.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- FK506结合蛋白5 (FKBP5) 已知其在毒症期间急性损伤中的作用.
- 在与败血症相关的肠损伤中,FKBP5的特定功能和机制尚不清楚.
- 这项研究调查了FKBP5在败血症模型中对肠道损伤的影响.
研究的目的:
- 阐明FKBP5在败血症引起的肠损伤中的作用.
- 检查FKBP5敲击对肠道屏障功能,炎症和亡的影响.
- 调查核因子kappa B (NF-κB) 信号传递在FKBP5中介作用中的参与.
主要方法:
- 已建立的小鼠败血症模型使用结和穿孔 (CLP).
- 使用了用脂多糖 (LPS) 刺激的Caco-2细胞模型.
- 评估了FKBP5对亡,屏障完整性标记物 (zonula occludens-1,occludin),炎症类细胞因子 (TNF-α,IL-6,IL-1β) 和NF-κB信号传递的淘汰效应.
主要成果:
- 在CLP和LPS治疗后,FKBP5表达在阴茎组织和Caco-2细胞中分别增加.
- 在败血症模型中,FKBP5敲击降低了亡,改善了肠道屏障功能,并降低了炎症标志物.
- 在体内和体外败血症模型中,FKBP5敲击抑制了NF-κB信号激活.
结论:
- 在败血症期间,FKBP5在促进炎症和肠道屏障功能障碍方面发挥着重要作用.
- 抑制FKBP5显示出对败血症引起的肠损伤的保护作用.
- 抑制NF-κB信号传递是通过FKBP5抑制发挥其保护作用的关键机制.
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