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抑制HMGB1通过ROS/AMPK/自途径减少TDI诱导的职业喘

Xiangjing Meng¹, Sumei Guo², Xiaoxia Zhang¹

¹Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250062, China.

Ecotoxicology and environmental safety

|October 15, 2023

概括

高流动性组盒1蛋白的抑制 (HMGB1) 通过减少炎症和气道过敏反应,缓解了小鼠的托二酸盐 (TDI) 诱导的喘. 这表明HMGB1是TDI诱导的肺部疾病的潜在治疗点.

科学领域:

肺部医学肺部医学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

二酸 (TDI) 暴露可能导致肺部疾病,如喘.
高流动性组盒1蛋白 (HMGB1) 抑制显示在人类支气管上皮细胞 (HBE) 中对TDI毒性产生保护作用.

研究的目的:

研究HMGB1在TDI诱导的小鼠喘中的体内作用.
探索暴露于TDI的HBE细胞中HMGB1的潜在分子机制.

主要方法:

在TDI诱导的喘小鼠模型中评估气道炎症,高反应性和重塑.
在实验室中对HBE细胞进行研究,以评估TDI诱导的活性氧物种 (ROS) 释放,炎症和自.
对蛋白质表达 (HMGB1,TLR4,维丁,MMP-9,E-cadherin) 和信号通路 (NF-κB,NLRP3炎症体) 的分子分析.

主要成果:

抑制HMGB1显著降低了TDI-喘小鼠的呼吸道炎症,高反应性和重塑.
在体外,HMGB1抑制降低了HBE细胞中的ROS释放,炎症和自活化.
抑制HMGB1调节了关键的分子标,包括TLR4,NF-κB,NLRP3炎症体和E-cadherin,并且与ROS/AMPK/自途径有关.

结论:

HMGB1在TDI诱导喘的发病过程中发挥着关键作用.
抑制HMGB1通过向ROS/AMPK/自途径,为TDI诱导的喘提供了潜在的治疗策略.
自激活可以加剧TDI诱导喘中的NLRP3炎症酶激活.

关键词:

呼吸道的炎症呼吸道的炎症喘喘是一种自自是一种自的过程.高流动性小组第1框高流动性小组第1框托卢烯二异酸盐是什么?

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