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阿佩林-13对呼吸机引起的急性肺损伤的保护作用

Siyu Lian¹, Xianming Zhang², Yi Shen¹

¹Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.

Molecular biology reports

|January 4, 2024

概括

通过减少炎症,亡和氧化应激,阿佩林-13的使用可以缓解大鼠的呼吸器诱导肺损伤 (VILI). 这项研究证明了阿佩林-13的存在.

科学领域:

肺部医学肺部医学
临界护理医学临界护理医学
分子生物学分子生物学

背景情况:

机械呼吸 (MV) 对于生命支持至关重要,但可能导致呼吸器诱导的肺损伤 (VILI).
维利病变包括炎症,氧化应激和亡,但尚未完全理解.
阿佩林/APJ轴是一个内源性机制,可以在急性呼吸窘迫综合征 (ARDS) 期间抵消损伤.

研究的目的:

在VILI的老鼠模型中研究apelin-13的保护作用.
为了确定阿佩林-13是否通过抑制炎症,亡和氧化应激来减轻VILI.

主要方法:

建立了一个VILI老鼠模型,使用高潮量通风4小时.
通过qRT-PCR,免疫光学和西部涂抹评估了阿佩林/APJ轴激活.
通过病理染色评估肺损伤,W/D比,BALF蛋白,炎症细胞因子 (IL-1β,IL-6,TNF-α) 和氧化应激标志物 (MPO,CAT,MDA).

主要成果:

在VILI大鼠肺部,阿佩林-13治疗激活了阿佩林/APJ轴.
阿佩林-13减少了肺组织的病理损伤,并逆转了与亡相关的蛋白质表达 (Bax,Bcl-2).
炎症性细胞因子水平降低,而抗氧化活性 (CAT) 增加,氧化应激标志物 (MDA) 降低.

结论:

在VILI过程中,阿佩林/APJ轴被激活.
过度表达的阿佩林-13提供了对VILI的保护.
阿佩林-13通过减少肺炎,亡和氧化应激减轻VILI.

关键词:

申诉人13号的申诉在阿佩林/APJ轴上细胞灭亡 (apoptosis) 是一种死亡的过程.炎症炎症是一种炎症.氧化应激是一种氧化应激.呼吸机引起的急性肺损伤

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