To observe the effects of cultured cordyceps sinensis(cultured cordyceps Sinensis,Ccs) in the animal model of pulmonary fibrosis induced by bleomycin(BLM) on pulmonary interstitial fibrosis by TGFbeta1-Smad pathway，and explore the mechanism of treating pulmonary fibrosis.Methods:A total of 50 rats were randomly divided into a blank control Group 10，a bleomycin Group(BLM) 10，a bleomycin and Cordyceps sinensis Group(Ccs) 10，a blank plasmid Group 10，Smad3 SiRNA gene silencing rat+bleomycin mildew element+cordyceps sinensis Group(Smad3 siRNA+BLM+CCS) 10.tracheotomy injected bleomycin(5 mg) was used to replicate mouse pulmonary fibrosis model，the control group was given saline 1.25 mL/kg.Ccs Group on the day of the modelling began to stomach artificial cordyceps sinensis solution 5 g/(kg·d)，the blank plasmid group in the second day of the model for the rapid injection of empty particles of the tail vein(3 mL/kg).The Smad3 siRNA+BLM+CCS group was injected into the Smad3 siRNA plasmid(3 mL/kg) at the end of the day after the injection of CCS on a daily basis.The animals were executed on the 28th day.In the left lung tissue，hematoxylin-eosin(HE) staining was used to observe the degree of alveolar inflammation and pulmonary fibrosis，and the right lung was detected by RT-PCR to detect the E-cad of the upper and middle skin cells of lung homogenate，the α-SMA intercellular markers and the signaling pathway related molecular Smad3，TGF-β1，CTGF Changes in the expression of mRNA protein.Results:In BLM Group，the degree of fibrosis was heavy，the degree of inflammation in the CCS group decreased markedly，the fibrous tissue was greatly reduced，and the degree of alveolar inflammation and fibrosis in Smad3 SiRNA+BLM+Ccs group was worse than that in CCS group.The results of RT-PCR showed that TGF-β1 and α-SMA expression in BLM group increased significantly The expression of α-SMA,and CTGF in SiRNA+BLM+CCS group increased significantly compared with that in CCS group.Conclusion:CCS may inhibit the occurrence of pulmonary fibrosis by blocking the TGFbeta1-Smad signaling pathway and reduce the effect of pulmonary fibrosis by inhibiting the activation of the TGFbeta1-Smad signaling pathway.