ObjectiveTo investigate the protective effect of ellagic acid （EA） against bleomycin （BLM）-induced pulmonary fibrosis and associated pulmonary function impairment in mice， and to elucidate its relationship with the regulation of the interleukin（IL）-17/ nuclear factor （NF）-κB/ matrix metalloproteinase （MMP）9 signaling axis. MethodsA pulmonary fibrosis model was established in male C57BL/6J mice via intratracheal BLM injection. Interventions included IL-17 neutralizing antibody， Ixekizumab， SB-3CT， PDTC， or EA were used to modulate the IL-17/NF-κB/MMP9 signaling axis. Pathological changes in lung tissue were observed via HE， Masson， and Sirius red staining. Pulmonary function was assessed using a pulmonary function test （PFT）. Western blot and qRT-PCR were employed to detect related protein and gene expression. Network pharmacology was utilized to predict the potential targets of EA. A protein-protein interaction （PPI） network was constructed using the STRING database and Cytoscape. Molecular docking was performed to validate the binding capability of EA to core targets. ResultsBLM successfully induced obvious pulmonary fibrosis and lung dysfunction in mice， significantly elevating the level of the pro-inflammatory cytokine IL-17. This was associated with the activation of the transcription factor NF-κB p65， leading to the upregulation of the pro-fibrotic factor MMP9. Inhibition of the IL-17/NF-κB/MMP9 signaling axis markedly alleviated the degree of pulmonary fibrosis. EA intervention significantly suppressed the BLM-induced increase in IL-17， blocked the activation of the NF-κB/MMP9 pathway， and consequently reduced lung fibrotic lesions and improved pulmonary function. ConclusionEA may effectively ameliorate BLM-induced pulmonary fibrosis and lung dysfunction in mice， likely by inhibiting the inflammatory and fibrotic responses mediated through the IL-17/NF-κB/MMP9 signaling pathway.