Salvianolic Acid A Attenuates Lipopolysaccharide‐Induced Acute Lung Injury by Activating AMPK/SIRT1/Nrf2 Signaling Pathway

ABSTRACT Salvianolic acid A (Sal A) has been reported to have anti‐inflammatory and antioxidant properties. The present study aimed to explore the potential mechanisms of Sal A on lipopolysaccharide (LPS)‐induced acute lung injury (ALI). The results indicated that Sal A pretreatment attenuated LPS induced lung injury, shown by alleviated histopathological damage and alveolar‐capillary barrier dysfunction, as well as reduced inflammatory response and oxidative stress. Moreover, Sal A pretreatment effectively increased the expression of p‐AMPK 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. In conclusion, these results indicated that Sal A exerted its protective effects on LPS‐induced ALI through suppressing inflammation and oxidative stress, which was mainly dependent on the activation of AMPK/SIRT1/Nrf2 signaling pathway.