Knockdown of MBD2 Attenuates LPS-Stimulated Inflammation and Apoptosis in WI-38 Cells Through the STAT-3 Pathway.

Abstract

This study aims to investigate the role of MBD protein 2 (MBD2) in the pneumonia cell model of lipopolysaccharide (LPS)-stimulated WI-38 cells and to uncover the mechanism. LPS-stimulated WI-38 cells were constructed as an in vitro pneumonia model. Quantitative polymerase chain reaction (qPCR) and immunoblot assays showed MBD2 expression in WI-38 cells. Cell counting kit-8 (CCK-8) assays showed the growth of WI-38 cells. Flow cytometry assays showed the apoptosis of WI-38 cells after LPS treatment and siRNA transfection. Enzyme-linked immunosorbent assay (ELISA) and qPCR assays showed the effects on inflammation, and immunoblot assays further confirm the mechanism. MBD2 was highly expressed in LPS-stimulated WI-38 cells. Knockdown of MBD2 alleviates production of cellular inflammatory cytokines in LPS-stimulated WI-38 cells. Further, knockdown of MBD2 alleviates apoptosis in LPS-stimulated WI-38 cells. Mechanically, the knockdown of MBD2 regulates the signal transducer and activator of transcription (STAT)-3 pathway in LPS-stimulated WI-38 cells. Knockdown of MBD2 attenuates LPS-stimulated inflammation and apoptosis in WI-38 cells through the STAT-3 pathway. Therefore, MBD2 could serve as a promising target of pediatric pneumonia.