Network pharmacology analysis of the therapeutic mechanisms of wintersweet bud against sleep disorders

Background: Sleep disorders are prevalent conditions associated with complex neurobiological disturbances, including inflammation, oxidative stress, circadian rhythm dysregulation, and hormonal imbalance. Wintersweet bud (Chimonanthus praecox), a traditional Chinese medicinal herb, has long been used for calming and sleep-promoting purposes; however, its molecular mechanisms in treating sleep disturbances remain unclear. Methods: A network pharmacology approach was employed to explore the potential mechanisms of Wintersweet bud in sleep disorders. Active compounds were screened based on drug-likeness criteria, and potential targets were obtained from public databases. Protein-protein interaction (PPI) analysis, hub gene identification, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed. A “Disease-Drug Component-Core targets-KEGG Pathways” network was constructed to illustrate the relationships among compounds, targets, and signaling pathways. Results: Three core compounds were identified, including Indole, Farnesyl acetate, and Fraxinellone. PPI analysis revealed ten hub genes, including ESR1, STAT3, PPARG, PTGS2, HIF1A, AR, FGF2, EP300, CD274, and KAT2B. GO enrichment indicated involvement in biological processes related to oxygen response, hormone regulation, and transcriptional regulation. KEGG analysis highlighted multiple pathways, with Tryptophan metabolism as the most significant metabolic pathway, along with Neuroactive ligand-receptor interaction and PI3K-Akt signaling pathways. Conclusions: Wintersweet bud may improve sleep disorders through multi-target and multi-pathway regulation involving metabolic modulation, neuroinflammatory control, and transcriptional regulation. These findings provide mechanistic insights supporting its potential as a complementary therapy for sleep disorders.