Erastin induces ferroptosis in lung fibroblasts through MAPK mediated oxidative stress signaling pathway
10.19405/j.cnki.issn1000-1492.2024.05.012
- VernacularTitle:Erastin通过MAPK介导的氧化应激信号通路诱导肺成纤维细胞铁死亡
- Author:
Yiran WANG
1
;
Shijie ZHANG
;
Yubo GUAN
;
Miaomiao LI
;
Ruyi CAI
;
Qi WU
Author Information
1. 徐州医科大学生理学教研室,徐州 221004
- Keywords:
pulmonary fibrosis;
lung fibroblasts;
ferroptosis;
reactive oxygen species;
MAPK signaling pathway
- From:
Acta Universitatis Medicinalis Anhui
2024;59(5):820-825
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism by which Erastin affects ferroptosis in lung fibroblasts.Meth-ods Mouse lung fibroblasts (C57/B6-L) were treated with varying concentrations of the iron death inducer Eras-tin.Cell viability was assessed using the cell counting Kit-8 (CCK-8) assay.Oxidative stress levels were visualized 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.Results 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 ac-tivity in lung fibroblasts (P<0.05).Conclusion It can be concluded that Erastin induces ferroptosis in lung fi-broblasts, potentially through the mediation of oxidative stress via the MAPK signaling pathway.
