急性肺损伤（ALI）是临床常见危重症，目前缺乏有效治疗手段，病死率可高达70%。肺部炎症失控和微血管通透性增加是ALI发病的重要机制。米托蒽醌甲磺酸盐（MitoQ）是一类靶向线粒体的抗氧化剂，可清除活性氧，抑制过氧化反应，保护线粒体，从而减轻细胞氧化应激。本课题利用脂多糖LPS建立的ALI小鼠模型，研究MitoQ对ALI的保护作用和相关机制。体外建立肺血管内皮细胞损伤模型，进一步探讨MitoQ对线粒体功能的修复作用，对细胞炎症和氧化应激的影响。同时深入阐明肺血管内皮细胞炎症相关的Toll样受体和代谢相关的PPARγ受体在内皮损伤中相互调节关系。本研究将有助于为治疗急性肺损伤提供新的手段。

Acute lung injury (ALI) is one of common severe disorders in clinic. Its mortality was up to 70% due to lack of effective treatment. The uncontrolled lung inflammation and increased pulmonary microvascular permeability are the key pathogenesis of ALI. MitoQ is one of typical mitochondrial antioxidants which can mitigate cellular oxidative stress by means of clearing reactive oxygen species, inhibiting peroxidation reaction and protecting the mitochondria. In this study, we will establish the LPS-induced ALI mouse model to investigate the protective role of MitoQ and its related mechanisms. Using a cellular injury model of pulmonary vascular endothelial cells, we will explore the effect of MitoQ on mitochondrial resuscitation, cellular inflammation and oxidative stress. Furthermore, the relationship between inflammation-related toll-like receptors (TLR) and the metabolism-related peroxisome proliferator-activated receptor γ (PPARγ) will be revealed in the vascular endothelial cells. The present project will provide potentially novel therapy for ALI.