佩奥尼佛林通过通过TLR4/NF-κB通路重新编程巨细胞极化来减轻败血症引起的肝损伤
Zhiwei Rong1,2, Baitian Li3, Chunzheng Liu2
1Postgraduate Training Base of Jinzhou Medical University, Shanghai East Hospital, Shanghai, China.
Frontiers in immunology
|February 5, 2026
概括
佩奥尼佛洛林通过转移巨细胞两极分化并抑制TLR4/NF-κB通路来防止败血症相关的肝损伤 (SALI). 这种天然化合物显示出作为SALI的新型免疫调节疗法的希望.
科学领域:
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
- 肝病学 肝病学是一种肝病学.
背景情况:
- 败血症相关的肝损伤 (SALI) 是一种严重的疾病,死亡率高,向治疗有限.
- 天然化合物Paeoniflorin具有抗炎和免疫调节特性,但其在SALI中的作用尚不清楚.
研究的目的:
- 在毒引起的肝损伤的小鼠模型中研究Paeoniflorin的保护作用和潜在机制.
- 阐明Paeoniflorin对巨细胞极化和SALI中的TLR4/NF-κB信号通路的影响.
主要方法:
- 一种结和刺穿 (CLP) 模型被用于诱导小鼠的多微生物败血症.
- 小鼠接受了不同剂量的Paeoniflorin治疗,并通过生物化学,组织学和亡测定来评估肝损伤.
- 使用包括RNA测序在内的分子和细胞技术分析了巨分极,炎症性细胞因子表达和TLR4/NF-κB通路激活.
主要成果:
- 佩奥尼佛洛林剂量依赖性降低了肝损伤标志物 (ALT,AST),组织病理损伤和肝细胞亡.
- 佩奥尼佛洛林降低了促炎性细胞因子的调节,并将巨细胞极化从M1转移到M2表型.
- 佩奥尼佛林抑制了TLR4/NF-κB信号通路,这种效应被TLR4激动剂逆转.
结论:
- 佩奥尼佛林通过通过TLR4/NF-κB通路抑制促进抗炎M2巨体表型来保护SALI.
- 佩奥尼佛洛林代表了因败血症引起的肝损伤的潜在治疗候选者.
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