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乙醇诱导的肺内Nrf2抑制是由AP-1驱动的miR-144表达介导的

Viranuj Sueblinvong¹, Xian Fan¹, Justin Guo¹

¹Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.

Alcohol, clinical & experimental research

|May 30, 2025

概括

乙醇增加了肺中的miR-144,通过抑制Nrf2.2,抑制了抗氧化防御. 准miR-144可能会防止与酒精有关的肺部疾病.

科学领域:

肺部医学肺部医学
分子生物学分子生物学
毒理学毒理学毒理学

背景情况:

酒精使用障碍 (AUD) 增加了肺部疾病的风险.
乙醇通过抑制核因子红色素2相关因子2 (Nrf2) 抑制肺的抗氧化和免疫功能.
以前的研究将艾滋病毒与通过肺中的miR-144抑制Nrf2联系起来.

研究的目的:

调查乙醇是否通过诱导肺组织中的miR-144来类似地抑制Nrf2.
阐明乙醇对Nrf2和肺防御的作用背后的分子机制.

主要方法:

在暴露于乙醇的老鼠肺部和分离的肺细胞 (AEC,AMs,PLF) 中量化miR-144表达.
在肺纤维细胞 (PLF) 中评估AP-1激活 (c-Fos,c-Jun) 使用西方免疫栓塞.
利用c-Fos沉默RNA和AP-1抑制剂来检查AP-1,miR-144和Nrf2之间的联系.
评估了调节miR-144对乙醇处理的PLF中Nrf2和抗氧化剂表达的影响.

主要成果:

长期食乙醇和直接暴露于乙醇增加了老鼠肺和肺细胞 (AEC,PLF) 中的miR-144表达.
在PLF中,乙醇诱导的AP-1激活 (c-Fos,c-Jun),AP-1抑制阻断了乙醇诱导的miR-144.
制c-Fos或抑制miR-144恢复了乙醇处理的PLF中的Nrf2和抗氧化剂 (GCLC,NQO-1) 表达.
单独过度表达miR-144可以模仿乙醇对Nrf2和抗氧化剂的抑制作用.

结论:

乙醇通过AP-1激活诱导肺部miR-144的表达.
这一途径有助于乙醇诱导的Nrf2抑制和抑制抗氧化剂/免疫防御.
miR-144代表了一种潜在的治疗标,用于减轻AUD患者的肺炎.

关键词:

在AP-1中,AP-1是AP-1.Nrf2 没有任何问题.酒精酒精酒精酒精酒精酒精酒精酒精肺肺肺肺肺肺肺肺肺在 miR-1444 中.

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