Exploring the mechanisms of luteolin in treating polycystic ovary syndrome and endometriosis via network pharmacology, molecular docking, and molecular dynamics simulation.

This study aims to elucidate the molecular mechanisms underlying luteolin's therapeutic effects on polycystic ovary syndrome (PCOS) and endometriosis (EM), thereby providing a theoretical foundation for developing novel treatment strategies. An integrated approach combining network pharmacology, molecular docking, and molecular dynamics simulation was employed. Potential targets of luteolin intersecting with PCOS/EM pathogenesis were identified through database mining, followed by the construction of a protein-protein interaction network to screen hub genes. Mechanistic insights were further explored through bioinformatics validation, gene enrichment analysis, molecular docking verification, and molecular dynamics simulations. Luteolin exerted synergistic therapeutic effects through core targets such as ESR1, MMP9, and ERBB2, mediated by triple pathways involving "nuclear receptor modulation-proliferation inhibition-metabolic improvement." Molecular docking and dynamics simulations confirmed its high binding stability and low binding free energy with key targets (e.g., ESR1, MMP9, and ERBB2). Additionally, the identification of shared risk genes between PCOS and EM offers novel targets for cross-disease interventions. Luteolin demonstrates significant potential in treating PCOS and EM through multi-target and multi-pathway mechanisms, aligning with the complex pathological networks characteristic of reproductive endocrine disorders. These findings provide a scientific rationale for its clinical translation.