Exploring the mechanism of galangin in alleviating alcoholic fatty liver disease based on the Gene Expression Omnibus database and network pharmacology

This study aimed to use the Gene Expression Omnibus (GEO) database combined with network pharmacology technology to investigate the positive effect of galangin on alcoholic fatty liver disease (AFLD) and explore its potential mechanism. The study first screened the differential genes in ALFD mice through the GEO database, obtained the possible targets of galangin through the SwissTargetPrediction and PharmMapper databases, and then obtained the intersection of drug and disease targets through a Venn diagram to build a “drug-target-pathway-disease” network relationship diagram, and its possible molecular mechanisms were analyzed through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. The network pharmacology analysis identified 22 potential targets for galangin in the treatment of AFLD, and protein-protein interaction network analysis revealed that the top 5 targets were protein kinase B (AKT) 1, epidermal growth factor receptor, mitogen-activated protein kinase (MAPK) 3, myeloid cell leukemia 1, and KIT proto-oncogene receptor tyrosine kinase. The KEGG results showed that the treatment of AFLD by galangin may be related to the MAPK signaling pathway, cyclic adenosine monophosphate signaling pathway, Ras-related protein 1 signaling pathway and phosphoinositide 3 kinase/AKT signaling pathway. Therefore, the combination of GEO database and network pharmacology prediction results showed that galangin could alleviate alcoholic fatty liver and exert anti-inflammatory effects. It provides a theoretical basis for research on the mechanism of galangin in treating AFLD and other diseases.