Objective To explore the underlying molecular mechanism of quercetin in tuberculous ulcer treatment using network phar-macology and molecular docking.Methods We identified quercetin drug targets by searching the PubChem,SwissTarget,and TargetNet databases,then combining our results with those of previous tuberculosis ulcer gene sequencing in our group,thereby obtaining inter-section targets.Using the DAVID database,we performed intersection target gene ontology functional enrichment analysis and signaling pathway enrichment analysis of the Kyoto gene and genome database.We analyzed the intersection target using the STRING database and Cytoscape software and screened the hub node.We used PyMOL and AutoDockTolls software to complete quercetin molecular docking with the hub node,then screened the core drug target of quercetin.Finally,we constructed a macrophage model to verify the above-men-tioned core genes.Results We screened overall 54 drug targets.Our enrichment analysis indicated that the signaling pathways involved in quercetin-mediated tuberculous ulcer treatment were e.g.,metabolic pathways,lipid and atherosclerosis,or the MAPK signaling pathway.In addition,ALOX5,TNF,SRC,MMP9,and EGFRmight be the key genes in quercetin-mediated tuberculous ulcer treatment.Results of our cell culture experiment demonstrated that upon quercetin intervention,SRCand EGFRexpression increased significantly while that of MMP9decreased significantly in M1 and M2 macrophages.Conclusion Quercetin could potentially regulate macrophage polarization by influencing SRC,EGFR,and MMP9expression.