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机械应激诱导NOX2促进内皮功能障碍在呼吸机诱导的肺损伤: 潜在的治疗用奎尔丁

Tao Jiang^1,2, Yabing Zhang^3,4, Zhiye Guo¹

¹Institute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|May 20, 2025

概括

机械通风可以通过NOX2.2通过增加活性氧物种 (ROS) 引起肺损伤. 抗氧化剂奎尔素通过抑制ROS通路来防止这种呼吸器诱导的肺损伤 (VILI).

科学领域:

生物医学工程生物医学工程
肺部医学肺部医学
细胞生物学细胞生物学

背景情况:

机械通风 (MV) 对于呼吸支至关重要,但可以诱导呼吸器诱导的肺损伤 (VILI).
VILI涉及内皮屏障的破坏,与高反应性氧物种 (ROS) 相关.
NADPH氧化酶2 (NOX2) 被确定为破坏内皮结的ROS的关键来源.

研究的目的:

调查NOX2及其下游信号在VILI中的作用.
评估抗氧化剂奎尔丁对VILI的保护作用.

主要方法:

使用小鼠和细胞培养物的VILI体内和体外模型.
评估NOX2表达,ROS水平和内皮结蛋白.
对CaMKII/ERK1/2信号通路的分析.
欧米克斯的数据分析比较了VILI和Cecal Ligation and Puncture (CLP) 模型.
在预防和治疗VILI时评估奎尔丁的疗效.

主要成果:

高循环拉伸 (CS) 和MV增加NOX2表达和ROS,导致内皮屏障功能障碍.
NOX2激活了依赖ROS的CaMKII/ERK1/2信号通路.NOX2激活了依赖ROS的CaMKII/ERK1/2信号通路.
奎尔素有效地清除ROS,防止机械拉伸诱导的内皮功能障碍.
在VILI和CLP模型中的基因表达模式显示了相似之处.
奎尔塞丁在服用前,通过抑制ROS/CaMKII/ERK1/2轴,提高了小鼠的生存率.

结论:

NOX2衍生的ROS和CaMKII/ERK1/2通路是VILI的关键调解者.
奎尔因通过向这一途径,显示出对VILI的显著保护作用.
奎尔可以预防MV诱导的肺损伤,并减轻现有的炎症诱导的肺损伤.

关键词:

在NADPH氧化酶 (NOX) 中.内皮壁障碍的功能障碍是内皮壁障碍.脑内皮细胞 (ECs) 是一种内皮细胞.机械应力机械应力机械应力机械传导机械传导文素 (Quercetin) 是一种文素.反应性氧物种 (ROS) 是一种反应性氧物种.呼吸器引起的肺损伤 (VILI)

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