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通过TLR4/NF-κB/mincle激活M1巨细胞对于三胺诱导的肝毒性至关重要

Ruoting Ding¹, Qingfeng Miao², Xindi Ma³

¹Department of Pharmacology, The Key Laboratory of Pharmacology and Toxicology for New Drugs, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, PR China; Department of Pharmacy, The Third Hospital of Shijiazhuang, Hebei, PR China.

Journal of ethnopharmacology

|December 31, 2025

概括

特里普托利德通过TLR4/NF-κB/Mincle通路激活M1巨细胞,导致肝损伤. 准Mincle可能会减少Triptolide的使用.

科学领域:

免疫学免疫学免疫学
毒理学毒理学毒理学
药理学药理学是指药理学的学科.

背景情况:

来自Tripterygium wilfordii的Triptolide (TP) 具有抗瘤特性,但严重的肝毒性限制了其使用.
了解TP诱导的肝损伤机制对于临床安全至关重要.

研究的目的:

研究M1巨分化在Triptolide诱导的肝毒性中的作用.
阐明底层的分子机制.

主要方法:

在接受TP治疗的小鼠中检查了Mincle表达和TLR4/NF-κB/Mincle通路的激活.
使用了Mincle淘汰赛模型和体外巨细胞炎症模型.
在AML12细胞上评估TP刺激的巨细胞超眠剂的影响.

主要成果:

通过TLR4/NF-κB/Mincle通路激活驱动的M1巨细胞极化,TP诱导肝损伤.
敏克尔淘汰赛显著逆转TP诱导的肝毒性.
由TP刺激的巨细胞释放了损害肝细胞的因素,增加了SAP130并损害了自.

结论:

通过TLR4/NF-κB/Mincle通路激活M1巨细胞对于TP肝毒性至关重要.
米克尔是一个潜在的治疗点,可以减轻Triptolide的肝脏毒性.

关键词:

肝毒性肝毒性肝毒性巨细胞的两极分化这是一个小小的小米.在 TLR4 中,三托利化物是什么

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