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甲基prednisolone通过调节miR-151-5p/USP38通路来缓解败血症中的肺损伤

Zhize Yuan¹, Qiuyun Wang², Yongchang Tan²

¹Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai 200433, China.

International immunopharmacology

|June 30, 2024

概括

甲基prednisolone (MP) 通过减少炎症和亡来治疗急性肺损伤 (ALI). 它通过抑制miR-151-5p来起作用,从而激活USP38,促进膜细胞的增殖.

科学领域:

肺部医学肺部医学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

急性肺损伤 (ALI) 涉及肺血管透性和气体交换受损.
甲基prednisolone (MP) 用于ALI减少炎症,但其机制是不清楚的.
脂聚糖 (LPS) 是ALI模型的常见诱导物.

研究的目的:

为了研究甲基prednisolone (MP) 的分子机制在治疗急性肺损伤 (ALI) 诱导的脂聚糖 (LPS).
探索miR-151-5p和USP38在MP对ALI治疗效果中的作用.

主要方法:

使用EDU,CCK-8和Annexin V/PI试验评估了膜II型上皮细胞 (AECII) 的增殖,活力和亡.
通过RT-qPCR量化miR-151-5p表达和USP38蛋白质水平通过西方布洛特.
使用ELISA进行细胞因子测量和ChIP-PCR/双露西法酶试验来确认miR-151-5p和USP38的相互作用.

主要成果:

在ALI模型中,MP改善了肺功能,减少了炎症,并增强了AECII扩散.
在AECII中,LPS增加了miR-151-5p,而MP治疗降低了它.
MP增加了USP38水平,这是miR-151-5p的下游目标. 抑制miR-151-5p或过度表达USP38模仿了MP的保护作用.

结论:

在AECII中,MP减轻了LPS诱导的炎症和亡.
通过抑制miR-151-5p和激活USP38.38,MP促进了AECII的扩散.

关键词:

在 AECII AECIIII 中.急性肺损伤是什么?急性肺损伤是什么?甲基普雷迪尼索隆 (Methylprednisolone) 是一种可以在 miR-151-5p 中.

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