Revealing the Mechanisms of Byu dMar 25 in the Treatment of Alzheimer’s Disease through Network Pharmacology, Molecular Docking, and In Vivo Experiment

Background: Alzheimer’s disease (AD) is the most common neurodegenerative disease, severely reducing cognitive level and life quality of patients. Byu dMar 25 (BM25) has been proved to have a therapeutic effect on AD. However, pharmacological mechanism still unclear. Therefore, this study aims reveal potential BM25 affecting AD from perspective network pharmacology experimental validation. Methods: The active ingredients were obtained TCMSP database literature. Possible targets predicted using SwissTargetPrediction tools. AD-related genes identified by GeneCards, OMIM, DisGeNET, Drugbank databases. candidate extraction intersection network. Additionally, “drug–target–disease” was constructed Cytoscape 3.7.2 for visualization. PPI STRING database, core modules filtered 3.7.2. Enrichment analysis GO KEGG carried out in Metascape platform. Ledock software used dock critical components with target. Furthermore, protein levels evaluated immunohistochemistry. Results: In study, 112 components, 1112 genes, 3084 functions, 277 pathways obtained. Molecular docking showed that effective treating β-asarone hydroxysafflor yellow A. important APP, PIK3R1, PIK3CA. indicated Golgi genetic regulation, peroxidase activity phosphatidylinositol 3-kinase complex IA, 5-hydroxytryptamine receptor complexes, cancer pathways, neuroactive ligand–receptor interactions played vital roles against rat experiment verified affected PI3K-Akt pathway activation Conclusions: This reveals pharmacology, which provides foundation further molecular treatment.