〔Abstract〕 Objective To investigate the effect of Naringin(NAR) on bleomycin-induced pulmonary fibrosis in mice and its possible mechanism. Methods Sixty male ICR mice were randomly divided into Control group,Model group,dexamethasone group(DXM,3 mg/kg),low-dose naringin group(L-NAR,25 mg/kg) and high-dose naringin group(H-NAR,100 mg/kg),with 12 mice in each group.Mouse pulmonary fibrosis model was established by intratracheal one-time infusion of bleomycin(5 mg/kg),and mice were sacrificed after 4 weeks of drug intervention.Lung mass was taken and lung index was calculated.Levels of hydroxyproline(HYP) in lung tissue were detected by alkaline hydrolysis.The pathological changes of lung tissues were observed and scored by HE staining.The degree of pulmonary fibrosis was observed and scored by Masson staining.The levels of IL-1β,IL-18,TGF-β1 in lung tissue were detected by ELISA.The expression levels of NLRP3,ASC and caspase-1 mRNA in lung tissues were detected by RT-PCR.The protein expression levels of NLRP3,ASC,caspase-1,Collagen I,α-SMA,E-cadherin and Vimentin in lung tissues were detected by Western blot. Results Compared with the Control group,the Model group showed significant lung tissue damage and severe degree of fibrosis,the lung index and lung tissue contents of HYP,IL-1β,IL-18 and TGF-β1 increased.The mRNA and protein expression levels of NLRP3,ASC,caspase-1,as the well as the protein expression levels of Collagen I,α-SMA and Vimentin increased,while the expression levels of E-cadherin significantly decreased,and the difference was statistically significant(P<0.05).Compared with the Model group,the degree of lung injury and fibrosis were significantly improved in the DXM group and the H-NAR group.The lung index and lung tissue contents of HYP,IL-1β,IL-18 and TGF-β1 decreased.The mRNA and protein expression levels of NLRP3,ASC,caspase-1,as the well as the protein expression levels of Collagen I,α-SMA and Vimentin decreased,while the expression levels of E-cadherin increased,and the difference was statistically significant(P<0.05).However,there was no significant difference in relevant indicators between the L-NAR group and the Model group. Conclusion NAR can effectively inhibit bleomycin-induced pulmonary fibrosis in mice,and the mechanism may be related to the inhibition of NLRP3 inflammatory corpuscles activation.