Therapeutic effect and mechanism of Cardamonin on pulmonary fibrosis / 中国现代医生

ABSTRACT

@#Objective To observe the effect of Cardamonin(CDN)on pulmonary fibrosis in mice,and explore the effect of CDN on transforming growth factor-β1(TGF-β1)/Smad signaling pathway.Methods The mice were grouped into:Sham group,Bleomycin(BLM)group,low dose of Cardamonin(CDN-L)group,medium dose of Cardamonin(CDN-M)group,high dose of Cardamonin(CDN-H)group and Dexamethasone(DXM)group.Injectioning of BLM induce pulmonary fibrosis in mice,the lung index was measured.Enzyme-linked immunosorbent assay kit measured serum tumor necrosis factor-α(TNF-α)levels,the hydroxyproline(HYP)content in lung tissue was detectioned by kits.Pathological changes were observed by Htoxylin Eosin and Masson staining,and the level of genes related to TGF-β1/smad signaling pathway was detected by RT-PCR.Results Compared with the Sham group,the lung index,Szapiel score and Ashcroft score of the BLM group were significantly increased(P<0.05),and the degree of pulmonary inflammation and fibrosis was more severe.The levels of TNF-α in serum and HYP in lung tissue were increased(P<0.05),lung tissue TGF-β1[(1.02±0.21)vs.(3.25±0.14)],smad2[(1.00±0.05)vs.(1.59±0.20)],smad3[(1.00±0.06)vs.(1.59±0.20)],α-smooth muscle actin(α-SMA)[(1.00±0.10)vs.(2.15±0.10)and E-Cadherin[(1.01±0.16)vs.(0.57±0.09)]mRNA level decreased(P<0.05).The intervention of CDN-M and CDN-H could decrease the lung index,alleviate the inflammation and Pulmonary fibrosis,and decrease the levels of TNF-α and HYP(P<0.05).The expression of TGF-β1,smad2,smad3 and α-SMA in lung tissue of mice with pulmonary fibrosis was down-regulate.CDN-L had no significant effect,while CDN-H had similar effects to DXM.Conclusion Cardamonin may play an anti-fibrotic role by mediating epithelial-mesenchymal transition through the TGF-β1/Smad pathway.