To explore the molecular mechanisms underlying the therapeutic effect of Bushen Huoxue Formula in the treatment of idiopathic pulmonary fibrosis(IPF) using network pharmacology.Methods:The targets of active ingredients of Bushen Huoxue Formula and disease targets were identified by searching databases.A protein-protein interaction(PPI) network was constructed，and gene ontology(GO) functional and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed.A biological network was constructed，and molecular docking was conducted to validate the key targets.The binding affinities of pirfenidone and nintedanib to the active ingredients and shared targets and pathways were compared.Further in vitro experiments were conducted for validation.Results:Fifty core targets，including caspase-3(CASP3)，tumor necrosis factor(TNF)，and c-Jun N-terminal kinase(JNK)，were identified.Eighty pathways were enriched，including the interleukin-17(IL-17) signaling pathway.Active ingredients such as wogonin and oroxylin A exhibited good molecular docking conformations.Furthermore，the active ingredients in Bushen Huoxue Formula，such as resveratrol，showed similar binding affinities to the key targets that had effect with pirfenidone and nintedanib.In vitro experiments demonstrated that Bushen Huoxue Formula exerted anti-fibrotic effects by inhibiting IL-17A，activating autophagy，and further degrading collagen.These findings validated some of the predictions made by network pharmacology.Conclusion:The targets of active ingredients and pathways in Bushen Huoxue Formula showed significant enrichment in inflammatory response，immunity，metabolism，etc.The anti-fibrotic effect of Bushen Huoxue Formula may be attributed to the inhibition of IL-17A expression，activation of IL-17A-mediated autophagy pathways，and degradation of collagen.