Astringin protects LPS-induced toxicity by suppressing oxidative stress and inflammation via suppression of PI3K/AKT/NF-κB pathway for pediatric acute lung injury.

Abstract

Acute lung injury (ALI) is a major pathophysiological problem defined by severe inflammation and acute disease with substantial morbidity and death. It is known that lipopolysaccharide (LPS) induces ALI by causing oxidative stress and inflammation. The goal of this study was to investigate the protective effect of astringin on LPS-induced ALI and probable pathways. Astringin is a stilbenoid, the 3-β-D-glucoside of piceatannol, mainly found in the bark of Picea sitchensis. The findings showed that astringin prevented LPS-induced cellular damage by reducing the generation of oxidative stress in LPS-stimulated A549 lung epithelial cells. Furthermore, astringin extensively decreased the production of inflammatory factors such as TNF-α, IL-1β, and IL-6. In addition, the western blot results revealed that the ability of astringin to reduce oxidative stress and the generation of inflammatory cytokines by inhibiting the ROS-mediated PI3K/AKT/NF-κB pathway could be the reason for its protective effect against LPS-induced ALI. Overall, the results suggest that astringin could be a possible inhibitor of ALI triggered by LPS for pediatric lung injury.