Network Pharmacology, Molecular Docking, and ExperimentalVerification Employed to Elucidate the Potential Mechanisms of BaziBushen Capsule for the Treatment of Premature Ovarian Failure

INTRODUCTION: The aim of this study was to investigate the mechanism of BZBS in the treatment of POF using network pharmacology and molecular docking, and to validate it through in vivo experiments. METHODS: Network pharmacology was used to construct chemical component-target pathway networks and protein-protein interaction networks to predict the potential targets of BZBS for the treatment of POF. The drug-target interactions were verified by molecular docking. Molecular dynamics simulations were performed to verify binding stability. Finally, experimental validation was performed. RESULTS: Network pharmacology analysis identified 220 BZBS compounds and 166 potential targets for POF treatment, with key core targets such as AKT1 and HIF-1α. Molecular docking showed that the main active ingredients of BZBS had a high affinity for POF, while molecular dynamics simulation verified stable interactions between AKT1 and Anhydroicaritin. It was confirmed that BZBS could ameliorate cisplatin CDDP-induced POF, regulate estrogen level, improve ovarian reserve, increase the expression of PI3K, AKT, HIF-1α, and VEGF proteins as well as immunofluorescence in ovarian tissues, and alleviate POF, which might be related to the activation of PI3K/AKT and HIF-1α/VEGF pathways. DISCUSSION: Through network pharmacology, molecular docking, molecular dynamics simulations, and in vivo experimental validation, it was preliminarily confirmed that BZBS ameliorates POF by activating PI3K/AKT and HIF-1α/VEGF pathways, which provides a theoretical basis for the subsequent studies on the treatment of POF with BZBS. However, our experiment lacks more in-depth clinical research. CONCLUSION: BZBS can improve symptoms of premature ovarian failure.