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两螺旋L37pA 保护肺血管内皮功能障碍,由截断的氧化脂通过与CD36受体的对抗性引起

Pratap Karki¹, Yue Li¹, Chen-Ou Zhang¹

¹Division of Pulmonary and Critical Care Medicine, Department of Medicine, and.

American journal of respiratory cell and molecular biology

|September 19, 2023

概括

截断的氧化脂 (Tr-OxPLs) 损害了肺部.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

截断的氧化脂 (Tr-OxPLs) 在病态状态下产生.
清理器受体CD36调解脂质运输并与Tr-OxPLs结合.
CD36和Tr-OxPLs与内皮功能障碍和急性肺损伤有关.

研究的目的:

调查CD36在调解由Tr-OxPLs诱导的肺内皮细胞 (EC) 功能障碍中的作用.
探索CD36抑制在Tr-OxPL诱导的肺损伤中的治疗潜力.

主要方法:

通过使用超内皮电阻和VE-cadherin免疫染来评估EC屏障破坏.
评估了一种针对CD36的 (L37pA) 对EC透性和炎症的影响.
使用CD36淘汰的小鼠和评估的肺损伤标记 (埃文斯蓝色试验,BAL液体分析).

主要成果:

Tr-OxPLs引起了急性EC屏障破坏和炎症激活.
L37pA显著减弱了Tr-OxPL诱导的EC透性,炎症,NF-κB激活和Src酶酸化.
CD36淘汰赛的小鼠对Tr-OxPL诱导的肺损伤表现出抵抗力,而L37pA治疗在体内改善了损伤.

结论:

CD36在调解Tr-OxPL诱导的肺EC功能障碍方面发挥着至关重要的作用.
CD36抑制代表了急性肺损伤和炎症的有前途的治疗策略.

关键词:

CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 L37pAA L37pAA L37pAA L37pAA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA L37pA 肺部急性肺损伤是什么内皮质功能障碍内皮质功能障碍截断的氧化脂酸.

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