YBX-1 alleviates sepsis-stimulated lung epithelial cell injury
Main Article Content
Keywords
acute lung injury, MAPK, oxidative stress, sepsis, YBX-1
Abstract
Objective: To explore the role of Y-box binding protein 1 (YBX-1) in the lipopolysaccharide (LPS)-stimulated inflammation and oxidative stress of BEAS-2B cell line and clarify the underlying mechanism.
Methods: LPS-stimulated BEAS-2B cells were used as a cell model of sepsis-stimulated acute lung injury (ALI). Immunoblot and quantitative polymerase chain reaction assays were used to detect the expression of YBX-1 in LPS-stimulated BEAS-2B cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, TdT-mediated dUTP nick end labeling, and immunoblot assays were conducted to determine the effects of YBX-1 on cell survival. JC-1 staining and adenosine triphosphate production were used to detect the effects of YBX-1 on mitochondrial function. Immunostaining and enzyme-linked immunosorbent serologic assay were performed to examine the effects of YBX-1 on the inflammation and oxidative stress of cells. Immunoblot assay was conducted to confirm the mechanism.
Results: YBX-1 was lowly expressed in LPS-stimulated BEAS-2B cells and enhanced the survival of LPS-stimulated lung epithelial cells. In addition, YBX-1 improved mitochondrial function of LPS-stimulated BEAS-2B cells. YBX-1 inhibited the inflammation and oxidative stress of LPS-stimulated BEAS-2B cells. Mechanically, YBX-1 inhibited mitogen-activated protein kinase (MAPK) axis, thereby alleviating sepsis-stimulated ALI.
Conclusion: YBX-1 alleviated inflammation and oxidative stress of LPS-stimulated BEAS-2B cells via MAPK axis.
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