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瓜可以通过抑制Rab5a介导的TLR4内部化在巨细胞中来缓解实验性类风湿性关节炎

Feilong Chen¹, Dingding Zhang², Lifang Cheng³

¹Department of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, PR China; Department of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, PR China.

Phytomedicine : international journal of phytotherapy and phytopharmacology

|July 4, 2024

概括

托尔类受体4 (TLR4) 内化,由Rab5a介导,在类风湿性关节炎 (RA) 中驱动巨细胞炎症. (XWG) 可以通过向这种途径来缓解关节炎,为RA提供了潜在的治疗策略.

科学领域:

免疫学免疫学免疫学
类风湿病学类风湿病学
药理学药理学是指药理学的学科.

背景情况:

类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,导致关节炎症和破坏.
巨细胞的炎症反应与RA的发病有关,而托尔类受体4 (TLR4) 的内部化可能起着关键作用.
在RA发展中TLR4内部化的具体作用仍然在很大程度上未被探索.

研究的目的:

阐明TLR4内化在RA相关的巨细胞炎症中的作用和机制.
调查TLR4内化是否是Xiaowugui (XWG) 的抗关节炎作用的关键调解者.

主要方法:

免疫光被用于评估TLR4和早期内体抗原1 (EEA1) 在RA患者的突样本和原诱导性关节炎 (CIA) 鼠标模型中的共同表达.
针对Rab5a的小干扰RNA (siRNA) 用于研究其对TLR4内化和巨细胞激活 in vitro的影响.
使用Rab5a淘汰赛小鼠 (Rab5a-/-) 来评估Rab5a在CIA中的体内作用.
分析了XWG蒸对CIA小鼠的治疗效果及其对巨细胞炎症通路的影响.

主要成果:

在RA患者和CIA小鼠中观察到TLR4和EEA1的共同表达和共同局部化的增加.
抑制TLR4内部化减少了LPS诱导的巨细胞炎症反应.
Rab5a沉默或遗传删除显著抑制了LPS诱导的TLR4内化,炎症性细胞因子产生 (IL-6,TNF-α) 和下游信号传递 (JNK,p65酸化).
在CIA小鼠中,XWG治疗缓解了关节炎,并抑制了Rab5a介导的TLR4内化和相关的炎症标志物.

结论:

通过一种新的Rab5a依赖途径,TLR4内化通过促进巨细胞炎症在类风湿性关节炎中发挥着显著的病原作用.
(XWG) 蒸对实验性关节炎表现出强大的治疗效果,可能是通过准Rab5a介导的TLR4内化机制.

关键词:

实现TLR4的内部化巨细胞是一个巨细胞.拉伯5a是第一个.类风湿性关节炎类风湿性关节炎类风湿性关节炎一个小瓜的脱剂.

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