Study on the mechanism of Bushen Ningxin Decoction in the treatment of premature ovarian insufficiency based on network pharmacology and molecular docking

GUO Qian; MA Weirong; CHEN Jie; WANG Haidan; TAN Yong

doi:10.13276/j.issn.2097-1656.2025.04.010

Abstract：Objective To explore the therapeutic targets of Bushen Ningxin Decoction in the treatment of premature ovarian insufficiency(POI).Methods The active ingredients of each drug in Bushen Ningxin Decoction were obtained by searching TCMSP and BATMAN-TCM databases.The disease targets of POI were collected through GeneCards,OMIM,PharmGKB and DrugBank databases.The active ingredients and disease gene targets were intersected to obtain the predicted targets of Bushen Ningxin Decoction in the treatment of POI.Cytoscape 3.8.0 was used to construct the"drug-component-target-disease"network.The protein-protein interaction network was constructed by STRING database and Cytoscape,and the core network was simplified.R software was used for GO enrichment and KEGG pathway enrichment analysis.The components with higher degree in the network were subjected to molecular docking with core targets.Results A total of 140 major active ingredients were screened,involving 272 gene targets.The major active ingredients included kaempferol,luteolin,quercetin,cryptotanshinone,tanshinone Ⅱa,sitosterol,stigmasterol,and angelicin.The core target genes included STAT3,TP53,ESR1,AKT1,MAPK1,RELA,etc.A total of 2 711 GO biological processes,102 cellular components and 293 molecular functions were enriched,including 188 KEGG signaling pathways such as fluid shear stress and atherosclerosis,MAPK,TNF,and IL-17.The results of molecular docking showed that the main active ingredients had good binding activity with the core targets.Conclusion Bushen Ningxin Decoction acts on key targets like STAT3,TP53,ESR1,AKT1,MAPK1,and RELA through active ingredients such as kaempferol,luteolin,quercetin,cryptotanshinone,tanshinone Ⅱa,sitosterol,stigmasterol and angelicin,playing a role through fluid shear stress and atherosclerosis,MAPK,TNF,IL-17 and other signaling pathways in the treatment of POI.