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在RIP1/3依赖的编程性亡诱导了败血症大鼠的肠道损伤
Acta biochimica et biophysica Sinica
|December 28, 2023
概括
由RIP1/RIP3驱动的编程细胞亡,有助于引起败血症的肠损伤. 抑制RIP1可以减少炎症,并通过减少ROS的产生来保护肠道.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 细胞死亡调节对于生理功能和败血症保护至关重要.
- 编程细胞亡与败血症的发病有关.
研究的目的:
- 为了研究已编程细胞亡在败血症引起的肠损伤中的作用和机制.
- 探索受体相互作用蛋白1 (RIP1) 和RIP3在这个过程中的参与.
主要方法:
- 通过Cecal-ligation和穿孔 (CLP) 的已建立的鼠标败血症模型和在IEC-6细胞上使用LPS的体外模型.
- 分析了RIP1,RIP3和MLKL的表达和酸化.
- 评估了RIP1抑制 (Nec-1) 和基因沉默 (si-RIP1,si-RIP3) 对细胞和组织损伤,细胞因子水平和活性氧物种 (ROS) 生产的影响.
主要成果:
- 在败血性大鼠皮质和LPS处理的IEC-6细胞中,RIP1的调节显著上升.
- Nec-1治疗降低了RIP1,p-RIP3和p-MLKL水平,缓解了肠道损伤,并降低了IL-6和TNF-α.
- 在IEC-6细胞中,LPS诱导了RIP1/RIP3的同位化,MLKL的化/转位,以及ROS的产生,而Nec-1,si-RIP1,si-RIP3和NAC减轻了这些影响.
结论:
- RIP1/RIP3依赖的编程细胞亡是败血症相关肠道损伤的关键因素.
- 这个过程与RIP1/RIP3介导的ROS产生有关,可以针对治疗干预.
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