Objective To reveal the mechanism of Yangxue Antai granules(YXATG)in the treatment of Recurrent spontaneous abortion(RSA)based on network pharmacology and molecular docking.Method The main chemical components and their targets of YXATG were collected from TCM Systematic Pharmacology Database and Analysis Platform(TCMSP)and TCM Integrated Pharmacology Research Platform(TCMIP)databases.The targets for RSA were identified from OMIM,GeneCards,Drugbank,PharmGkb and TTD databases.The intersection of drugs and disease targets was analyzed by drawing venn diagram,an online tool,and imported into the database,and analyzed the drug-disease target intersection through the online tool draw venn diagram,imported into STRING database,analysed the shared target interaction relationship(PPI),and performed bioinformatics analysis on it.In addition,the core targets of YXATG for RSA were analyzed according to Degree value,and molecular docking technology was used to study the binding degree between the targets and chemical components to validate the results of network pharmacological analysis.Results A total of 70 chemical components and 236 targets of YXATG were collected,and 453 disease targets were obtained after de-weighting.A total of 66 common targets were obtained by intersection analysis,and PPI interaction analysis revealed that IL6,MMP9,TNF,IL1B and IL10 were the core targets of YXATG for the treatment of RSA.Bioinformatics enrichment analysis revealed that these common targets mainly acted in TNF signaling pathway,HIF-1 signaling pathway,FoxO signaling pathway,estrogen signaling pathway and other signaling pathways.Further molecular docking results showed that the target MMP9 with the highest degree value docked well with paeoniflorin,sesamin,quercetin and kaempferol.Especially,paeoniflorin docked better than the positive control.Conclusion Through network pharmacology and molecular docking analysis,it was found that the main active ingredients in YXATG exerted their therapeutic effects on RSA by affecting multiple signaling pathways through their action on MMP9.
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