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臭氧预暴露通过ADAR1调节和热激活加剧了败血性肺损伤

Quanzhen Wang¹, Yajun Liu¹, Yuke Zhang²

¹Department of Critical Care Medicine, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.

International journal of toxicology

|November 13, 2025

概括

长期暴露于臭氧会通过改变ADAR1水平并增加热死来加剧败血症引起的肺损伤. 这项研究揭示了一种新的机制,它将臭氧,ADAR1和炎与败血症的病原性联系起来.

科学领域:

环境健康环境健康
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

长期暴露于臭氧会损害肺功能,增加败血症的严重程度.
热,一个被编程的细胞死亡途径,是败血症和肺部损伤的核心.
炎症酶激活将臭氧暴露与热死联系在一起.

研究的目的:

研究臭氧暴露加剧败血症引起的肺损伤的分子机制.
为了确定关键的调节基因,参与臭氧,败血症和烧死之间的相互作用.

主要方法:

对公共基因组数据的生物信息分析,以识别与热致死相关的基因以及受败血症和臭氧影响的基因.
在暴露于臭氧的小鼠中进行实验验证,随后发生脂多糖诱导的败血症.
评估肺组织损伤,炎症和热的标志物.

主要成果:

生物信息学发现了caspase-1,interleukin-1β和gasdermin D的上调,以及ADAR1.1的下调.
臭氧预暴露在败血症小鼠的肺部中加剧了炎症和卡斯帕-1-介导的烧亡.
ADAR1水平最初在败血症中增加,但随着臭氧共同暴露而下降,证实了生物信息学预测.

结论:

臭氧预暴露会通过调节ADAR1的表达和促进热致死,使败血性肺损伤恶化.
ADAR1-激素灭菌途径代表了在败血症期间臭氧诱导的肺损伤的一个新机制.
在这种情况下,ADAR1被确定为一个关键的调节分子.

关键词:

炎症酶激活的作用肺部受伤的原因是肺部受伤.暴露于臭氧的情况.热致灭 (pyroptosis) 是一种致的过程.这是一种血症.

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