Erastin induces ferroptosis in lung fibroblasts through MAPK mediated oxidative stress signaling pathway / 安徽医科大学学报

ABSTRACT

Objective @#To investigate the mechanism by which Erastin affects ferroptosis in lung fibroblasts.@*Methods@#Mouse lung fibroblasts (C57/B6⁃L) were treated with varying concentrations of the iron death inducer Erastin, Cell viability was assessed using the cell counting Kit⁃8 (CCK⁃8) assay. Oxidative stress levels were visualize using a fluorescence microscope , and the expression of proteins related to the mitogen⁃activated protein kinase (MAPK) signaling pathway was analyzed using Western blot. Additionally , the p38 and extracellular regulated protein kinase (ERK) inhibitors SB203580 and U0126 were employed to further elucidate the mechanism by which Erastin induces iron death in lung fibroblasts. @*@#At a concentration of 100 μmol/L , Erastin effectively in⁃duced ferroptosis in lung fibroblasts , leading to an upregulation of oxidative stress. Furthermore , the phosphoryla⁃tion levels of p38 and ERK proteins in the MAPK pathway were elevated (P < 0. 05) . The addition of SB203580 and U0126 inhibitors resulted in a significant reduction in oxidative stress levels and a notable increased in cell actiivity in lung fibroblasts (P < 0. 05) . @*@#It can be concluded that Erastin induces ferroptosis in lung fibroblasts , potentially through the mediation of oxidative stress via the MAPK signaling pathway.