Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice

Alcoholic liver disease (ALD) is a global that manifests in variety of forms, including alcoholic hepatitis, inflammation, fatty liver, and cirrhosis. One the early stages ALD (AFL) disease, which primarily characterized by accumulation lipids inflammation hepatocytes. Guanylate binding protein 5 (GBP5) has been investigated for its involvement progression. The regulatory effects GBP5 on progression AFL are still not well understood. This study aims to investigate impact underlying mechanism action. To achieve this, gene expression was evaluated using western blot reverse transcription quantitative polymerase chain reaction (RT-qPCR) methods. Lipid confirmed Oil Red O staining assay, while levels Triglyceride (TG), aspartate aminotransferases (AST), alanine (ALT) were measured commercial kits. inflammatory cytokines assessed enzyme-linked immuno sorbent assay (ELISA) assay. Finally, cell apoptosis flow cytometry. Cell through Our work demonstrated up-regulated Ethyl Alcohol (EtOH) group. Additionally, lipid increased after EtOH inducement, but this change attenuated silencing GBP5. Silencing reduced EtOH-mediated apoptosis. it discovered knockdown retarded EtOH-stimulated nuclear factor kappa-B (NF-κB) pathway. Knockdown alleviated inhibition NF-κB finding suggested may be useful bio-target treatment.