Objective To explore the therapeutic mechanism of ursolic acid against silicosis fibrosis based on network pharmacology, molecular docking and in vitro experiments. Methods Ursolic acid targets were obtained from databases, including GeneCards and PubChem. Disease-related databases (GeneCards, OMIM) were searched for targets related to silicosis fibrosis and epithelial-mesenchymal transition ( EMT). A micro-biotech platform was used to screen for intersecting targets, and a protein-protein interaction network was constructed using the STRING database and Cytoscape to screen the core targets. The David database was used for GO and KEGG enrichment analysis. AutoDock was used for molecular docking validation. Key targets were validated using beas-2B cells. ResultsWe obtained 179 ursolic acid targets, 8023 silicosis fibrosis targets, 6809 EMT-related targets, and 133 intersecting targets. Nine core targets, including AKT, STAT3, and MMP9, were identified, among which MMP9 and AKT had the highest connectivity in the protein-protein interaction network. Molecular docking showed that ursolic acid had strong binding activity with MMP9 ( binding energy - 8. 4 kJ/ mol) and AKT ( binding energy - 7. 9 kJ/mol). KEGG analysis indicated the PI3K-AKT signaling pathway to be a key regulatory pathway. In vitro experiments showed that ursolic acid significantly inhibited the decrease in cell viability induced by SiO2 (CCK8). Ursolic acid also reduced p-AKT expression (Western blot,P<0. 05); downregulated expression of the fibrosis marker α-SMA and the mesenchymal marker Vimentin, while upregulated expression of the epithelial marker E-cadherin (immunofluorescence / Western blot,P<0. 05). Conclusions Ursolic acid may play an anti-silicosis fibrosis role by inhibiting AKT phosphorylation, reducing MMP9 levels and regulating EMT.