Affiliation:
1. Department of General Surgery, Anhui No. 2 Provincial People's Hospital Anhui Medical University Hefei China
2. Department of Surgery The Second Affiliated Hospital of Jiaxing University Jiaxing China
Abstract
AbstractBackgroundAlcoholic hepatitis (AH) is a severe alcoholic‐related liver disease that is a leading cause of morbidity and mortality, for which effective treatments are lacking. Brain‐expressed X‐linked gene 2 (BEX2) has been implicated in various diseases, but its association with AH has received limited attention. Thus, this study investigated BEX2's impact on the progression of AH by affecting the c‐Jun NH2‐terminal kinase/mitogen‐activated protein kinase (JNK/MAPK) pathway.MethodsMicroarray dataset GSE28619 from the Gene Expression Omnibus database was used to identify differentially expressed genes in AH. Immunohistochemistry, terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labeling (TUNEL), Western blot analysis, and flow cytometry were used to measure various factors in the liver tissue of AH mice.ResultsBEX2 expression was significantly upregulated in the model. BEX2 gene silencing increased the levels of glutathione peroxidase and superoxide dismutase while decreasing malondialdehyde content; phosphorylation of JNK, c‐JUN, and p38MAPK; apoptosis rate; and the extent of JNK/MAPK pathway activation.ConclusionsThese findings provide valuable insights into the mechanisms underlying AH development and highlight the potential role of BEX2 gene expression as a promising therapeutic target for AH.