111 / 2021-10-24 11:32:55

Dieckol alleviates LPS-induced acute lung injury via inhibiting Keap1-Nrf2/HO-1 mediated ferroptosis

Dieckol,acute lung injury,Keap1-Nrf2/HO-1,ferroptosis

Acute lung injury (ALI) induces uncontrolled and self-mutilating pulmonary inflammation with high morbidity and mortality in critically ill patients. In recent years, many bioactive components extracted from marine drugs have been reported to effectively ameliorate ALI through different mechanisms. Ferroptosis is classified as regulatory cell necrosis, more immunogenic than apoptosis, and promotes the progression of ALI. In this study, we examined the regulation of Dieckol, isolated from seaweed, on the inflammatory response and ALI by ferroptosis. Our study found that administration of Dieckol protected mice against LPS-induced ALI, including significantly improved lung pathology, and decreased the extent of pulmonary edema, inflammation, and ferroptosis. In vitro, Dieckol inhibited LPS-induced ferroptosis and inflammation in RAW264.7 cells. These results show that ferroptosis mediates LPS-promoted inflammation in RAW264.7 cells and that Dieckol may ameliorate LPS-induced inflammation by inhibiting ferroptosis. Meanwhile, the Keap1-Nrf2/HO-1 pathway was regulated by Dieckol, and the anti-ferroptosis and inflammation in LPS-treated cells were significantly abolished by inhibiting the Keap1-Nrf2/HO-1 pathway.