基于网络药理学及分子对接技术研究黄芪治疗亚临床甲状腺功能减退症的分子机制OA

Objective:To investigate the molecular mechanism of Huangqi(Astragali Radix)in treating subclinical hypothyroidism based on network pharmacology and molecular docking.Methods:The main medicinal components of Huangqi were obtained from the BATMAN-TCM,TCM-ID,and TCMSP herbal component databases.Targets of Huanqi components were identified through TCMSP,Swiss TargetPrediction,and SwissADME platforms.Relevant targets for subclinical hypothyroidism were acquired from GeneCards,OMIM,and PharmGKB databases.The intersection of targets between Huangqi and subclinical hypothyroidism was obtained using Venny 2.1.0,and a"Huangqi-components-targets-subclinical hypothyroidism"network diagram was constructed with Cytoscape 3.1.0 software.Protein-protein interaction(PPI)networks of targets were generated using the STRING database,visualized with Cytoscape 3.1.0,and core targets were screened.GO gene function and KEGG signaling pathway enrichment analyses were performed using the DAVID database and microbial platforms.Pathway and target network diagrams were constructed with Cytoscape and SangerBox software.Molecular docking was performed on core targets and active components using PyMOL 2.3.4 and AutoDockTools 1.5.6 software.Results:There were 21 major medicinal molecules in Huangqi,with 44 overlapping targets between Huangqi and subclinical hypothyroidism.Among these,5 core targets were identified,namely EGFR,ESR1,TNF,MMP9,and PIK3CA.GO gene functional analysis revealed that core targets were involved in 40 biological processes,4 cellular components,and 6 molecular functions.KEGG pathway enrichment analysis identified 65 signaling pathways in cells associated with these overlapping targets.Molecular docking results demonstrated strong binding affinity with low binding energy for MMP9-isoflavones,MMP9-manghoshanin,PIK3CA-isoflavones,and TNF-rhamnolimonate.Conclusion:The medicinal components in Huangqi,such as isoflavonones,steviol glycosides,and rhamnocitronin,can treat subclinical hypothyroidism through multi-target and multi-pathway mechanisms.