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通过调节AXL介导的MAPK/NF-κB信号通路,C1632可以防止LPS引起的急性肺损伤

Yanan Mei¹, Yihang Wu¹, Yihui Zhai²

¹Respiratory Medicine Department, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

International immunopharmacology

|March 25, 2025

概括

通过向AXL受体和MAPK/NF-κB通路,C1632有效地治疗急性肺损伤 (ALI) 和急性呼吸困扰综合征 (ARDS). 这种新型治疗剂可以减少肺炎和损伤,而不会产生显著的毒性.

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.
肺部医学肺部医学

背景情况:

急性肺损伤 (ALI) 和急性呼吸困难综合征 (ARDS) 是具有高死亡率的危急疾病.
TAM受体AXL与先天性免疫和炎症反应有关.

研究的目的:

为了研究C1632的治疗疗效和机制,在一个小鼠模型的脂聚糖化物 (LPS) 诱导的ALI/ARDS.
评估C1632作为ALI/ARDS新疗法的潜力.

主要方法:

在LPS挑战之前,小鼠先用C1632进行预治疗.
评估了炎症标志物 (IL-6,TNF-α),粘附分子 (VCAM-1,ICAM-1),炎症细胞透和肺部组织病理学.
研究了C1632对AXL表达和MAPK/NF-κB信号通路激活的影响.
评估的C1632细胞毒性和器官毒性在体外和体内.

主要成果:

C1632预处理显著抑制LPS诱导的炎症因子产生和血管粘附分子表达.
C1632减少了炎症细胞的透,并减轻了肺部的病原体损伤.
C1632抑制了AXL转录和表达,抑制了LPS诱导的MAPK/NF-κB通路激活.
C1632在小鼠中没有显著的细胞毒性或损害肝脏和功能.

结论:

在ALI/ARDS中,AXL是通过MAPK/NF-κB信号通路调解的抗炎治疗的可行的治疗标.
C1632表明作为ALI/ARDS的安全有效治疗剂具有前途.

关键词:

一个AXL一个AXL 急性肺损伤是什么?急性肺损伤是什么?C163232 这是什么意思?炎症炎症是一种炎症.脂聚糖类糖化物脂聚糖类糖化物

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