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The present study aimed to explore the potential mechanisms of Sal A on lipopolysaccharide (LPS)\u2010induced acute lung injury (ALI). The results indicated that Sal A pretreatment attenuated LPS induced lung injury, shown by alleviated histopathological damage and alveolar\u2010capillary barrier dysfunction, as well as reduced inflammatory response and oxidative stress. Moreover, Sal A pretreatment effectively increased the expression of p\u2010AMPK and SIRT1 and promoted Nrf2 nuclear translocation in lung tissues. However, these effects were remarkably blunted by Compound C. Molecular docking experiments further confirmed that Sal A bound well to the active sites of AMPK and SIRT1. 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