Abstract
Acute respiratory distress syndrome (ARDS) refers to the injury of alveolar epithelial cells and capillary endothelial cells due to various injury factors. Research on the pathogenesis of ARDS has made great progress, but the exact pathogenesis of ARDS has not been fully elucidated. Up to now, the prevention and treatment of ARDS is still an important scientific problem that needs to be solved urgently. In this work, we analyzed the effect of uridine on ARDS. An ARDS model was successfully constructed by lipopolysaccharide (LPS) stimulation. Western-blotting, IFA, ELISA, RT-PCT and CLSM were conducted to investigate the effect of uridine on ARDS and insulin resistance, and the results showed that lung histopathological alterations were significantly attenuated by uridine treatment. Further work showed that the levels of proinflammatory cytokines were significantly down-regulated in the lung tissue after treatment with uridine. Additionally, the numbers of total cells and neutrophils in the bronchoalveolar lavage fluid (BALF) were also decreased in the uridine-treated ARDS mice. We further explored the potential mechanism by which uridine could treat ARDS, and the results indicated that NF-κB signaling was down-regulated by uridine treatment. Next, we studied insulin sensitivity in the ARDS mice, and found that insulin signaling was significantly down-regulated, and uridine could enhance insulin sensitivity in the ARDS mice model. Furthermore, we found that the levels of inflammation and oxidative stress were decreased by uridine treatment, which may be the potential mechanism by which uridine could improve insulin sensitivity. Taken together, the current work provides evidence that uridine can serve as a potential drug to treat ARDS and insulin resistance.