FOXA2 attenuates lipopolysaccharide‑induced pneumonia by inhibiting the inflammatory response, oxidative stress and apoptosis through blocking of p38/STAT3 signaling

• DOI: 10.3892/etm.2023.12168
• Publication Date: 2023-08-17T06:10:41Z
• Authors: Zhibin Xue; Yinglin Li; Shiji Xiao; Hanqing Zhang; Jianzhang Xu
• Keywords: FOXA2; Viability assay

Pneumonia is a severe inflammatory disease of the lung. Forkhead box protein A2 (FOXA2) has been demonstrated to serve an important regulatory role in various pulmonary diseases; however, FOXA2 pneumonia remains be elucidated. The present study aimed explore functional effects and mechanism pneumonia. An <em>in vitro</em> model was induced using lipopolysaccharide (LPS) WI‑38 cells. mRNA expression levels were determined by reverse transcription‑quantitative PCR western blotting, respectively. Cell viability assessed Counting Kit‑8 assay. Inflammatory cytokines evaluated ELISA kits oxidative stress markers malondialdehyde assay kit, superoxide dismutase kit CATalase kit. apoptosis flow cytometry caspase3 activity determined. Western blotting performed examine endoplasmic reticulum (ERS)‑associated factors. For rescue assay, p38 MAPK activator, U46619, used investigate involving p38/STAT3 signaling. downregulated LPS‑induced overexpression alleviated inflammation, stress, ERS Furthermore, inhibitory on apoptosis, as well cells partly weakened additional treatment with U46619. In conclusion, served protective against regulating signaling, providing novel idea for development targeted therapeutic strategies