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铁亡调解呼吸道上皮层E-cadherin功能障碍在LPS诱导的急性肺损伤中

Zemin Chen¹, Haixiong Tang², Sudan Gan¹

¹Department of Pulmonary and Critical Care Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Pulmonary pharmacology & therapeutics

|December 28, 2023

概括

铁亡,一种细胞死亡形式,在急性肺损伤 (ALI) 期间驱动呼吸道上皮细胞中的E-cadherin损失. 用liproxstatin-1抑制铁亡,可以防止ALI并恢复E-cadherin的功能.

科学领域:

细胞生物学细胞生物学
肺部医学肺部医学
病理生理学病理生理学

背景情况:

呼吸道上皮质中的E-cadherin损失有助于急性肺损伤和急性呼吸困扰综合征 (ALI/ARDS).
在ALI/ARDS中E-cadherin功能障碍背后的机制在很大程度上是未知的.
铁亡因其在ALI/ARDS病原发生中的作用越来越受认可.

研究的目的:

调查铁质在ALI/ARDS中呼吸道上皮质E-cadherin失调中的作用.
为了确定铁灭的抑制是否可以防止E-cadherin的损失,并防止ALI.

主要方法:

在BALB/c小鼠中通过脂聚糖化物 (LPS) 灌注建立了急性肺损伤 (ALI) 模型.
小鼠接受了铁灭抑制剂liproxstatin-1 (Lip-1) 或ferrostatin-1 (Fer-1) 的治疗.
分析了铁亡标记物,E-cadherin和可溶性E-cadherin (sE-cadherin) 的表达.

主要成果:

暴露于LPS减少了肺E-cadherin,减少了膜E-cadherin,并增加了SE-cadherin.
暴露于LPS的小鼠中的线粒体形态表明铁亡,铁的增加,MDA和GPX4的减少.
高剂量的Lip-1 (30 mg/kg) 保护了LPS诱导的肺损伤,并通过抑制铁亡,恢复了E-cadherin的表达.

结论:

铁灭症在LPS诱导的ALI中调解了呼吸道上皮层E-cadherin功能障碍.
向铁亡可能是ALI/ARDS的治疗策略.
利普洛克斯塔丁-1通过调节铁和E-cadherin,显示出对ALI的保护作用.

关键词:

急性肺损伤是什么?急性肺损伤是什么?气道上皮质气道上皮质这是E-cadherin.铁化是铁化的一种.这是一种Liproxstatin-1的药物.

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