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通过TLR4/MyD88/NF-κB p65途径缓解肺缺血-再输液损伤

Xiao-Rui Tian¹, Jun-Hui Zhao¹, Xia-Hui Yin¹

¹Department of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.

Phytotherapy research : PTR

|September 4, 2025

概括

通过抑制TLR4/ MyD88/ NF- kB通路,保护抗肺缺血再输伤. 在大鼠模型中,ASIV与TLR4- MD-2结合,减少炎症和细胞损伤.

科学领域:

药理学
免疫学
细胞生物学

背景情况:

肺缺血再输损伤 (PIRI) 是一个重要的临床挑战.
在之前的研究中,阿斯特拉加洛西德IV (ASIV) 已显示出对肺部损伤的保护作用.
需要进一步阐明ASIV保护作用的精确分子机制.

研究的目的:

通过抑制托尔类受体4 (TLR4) /MyD88/NF-κB p65信号通路来调查ASIV是否会减弱PIRI.
将ASIV与DEX和NAC等其他药物的保护效果进行比较.
为了阐明ASIV和TLR4-MD-2之间的结合相互作用.

主要方法:

使用氧气-葡萄糖剥夺/再氧化 (OGD/R) 诱导细胞损伤的体外研究.
在Sprague-Dawley大鼠体内PIRI模型,监测肺损伤标志物和氧化应激.
在mRNA和蛋白质水平上评估TLR4/MyD88/NF-κB p65通路的激活.
分子对接,结合亲和度计算和表面等离子体共振 (SPR) 来评估ASIV-TLR4-MD-2相互作用.

主要成果:

与DEX和NAC相比,ASIV对OGD/R诱导的细胞损伤有更好的保护,与TAK-242有协同作用.
在体内,ASIV治疗显著减少了肺组织损伤,减少了氧化应激标志物 (MDA,MPO) 和增加了抗氧化剂水平 (T-SOD,GSH-PX).
ASIV的使用导致TLR4,MyD88,NF- kBp65和p- NF- kBp65蛋白表达的显著下调.
分子对接预测了ASIV与TLR4-MD-2的强度结合 (自由结合能量为-8.0 kcal·mol-1),由SPR (K_D为2.17 × 10−6 M) 证实.

结论:

通过特别结合TLR4-MD-2,ASIV有效地减轻了PIRI.
这种结合抑制了TLR4/ MyD88/ NF- kB p65炎症通路的激活.
ASIV是缓解肺缺血再输液损伤的有希望的治疗药物.

关键词:

美国美国 TLR4-MD-2 其他保护作用

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