LAUSR

Abstract Ferroptosis is a newly discovered type of cell death that is different from other types of cell death morphologically and biologically. It is considered to play an important role in many pulmonary diseases. Currently, the regulatory roles of antioxidation in lung epithelial ferroptosis have not been fully explored. In this study, we show that resveratrol protected erastin-induced ferroptosis in BEAS-2B cells. Erastin led to increased reactive oxygen species production and iron deposition in BEAS-2B cells, which could be rescued by resveratrol. Furthermore, we observed that resveratrol led to modulating ferroptosis-associated gene glutathione peroxidase 4 expression and regulating glutathione in BEAS-2B cells. Resveratrol exerted an antioxidant property in erastin-induced ferroptosis of BEAS-2B cells by activating the nuclear factor-erythroid 2-related factor 2/Kelch-like ECH-associated protein signaling pathway. Finally, these findings demonstrate that resveratrol protects BEAS-2B from erastin-induced ferroptosis.