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Experimental Study Of Pirfenidone Alleviated Bleomycin-Induced Pulmonary Fibrosis In Mice By Inhibiting The TGF-β1/Smad2/3 Signaling Pathway

Posted on:2022-01-06Degree:MasterType:Thesis
Country:ChinaCandidate:J ZhongFull Text:PDF
GTID:2504306743486544Subject:Clinical Medicine
Abstract/Summary:PDF Full Text Request
Objective To investigate the effect of pirfenidone(PFD)on BLM-induced pulmonary fibrosis in mice and its mechanism.Methods BLM was used to construct the mice model of pulmonary fibrosis and PFD was used to treat the mice.Lung tissues of mice were stained with hematoxylin-eosin(HE)and Masson to observe the histopathological structure of the lungs.Immune organized method was used to determine type I collagen(Col-I)content;By transforming growth factor-β(TGF-β1)build the HLFs cells in vitro model,and using the PFD to process cells,the cell activity was evaluated by determined by MTT method,using the fluorescent quantitative PCR(q RT-PCR)and protein immunoblot method(Western blot)determination of type III collagen(Col-III)and alpha smooth muscle actin(α-SMA),fiber mucin(fibronectin),TGF-β1/Smad2/3 signaling pathways protein content.Results Compared with the Control group,the Model group showed inflammatory reaction and collagen fiber deposition in the lung tissues,and the levels of TNF-α,IL-6,Col-I,Col-III,α-SMA and fibronectin in the lung tissues of Model group were increased,and TGF-β1/smad2/3 signaling pathway was activated.After PFD treatment,the inflammatory response and collagen deposition were ameliorated in mice,and the levels of TNF-α,IL-6,Col-I,Col-III,α-SMA and fibronectin in the PFD group were significantly lower than those in the Model group(P<0.05),and the TGF-β1/smad2/3 signaling pathway activated by BLM was inhibited.TGF-β1treatment enhanced HLFs cell viability,promoted the expression of Col-III,α-SMA and fibronectin,activated TGF-β1/smad2/3 signaling pathway;the cell viability of PFD+TGF-β1 group was significantly lower than that of TGF-β1 group(P<0.05),the expression of Col-III,α-SMA and fibronectin in PFD+TGF-β1 group were significantly lower than those of TGF-β1 group(P<0.05),and the TGF-β1/smad2/3signaling pathway activated by TGF-β1 was inhibited.Conclusion PFD can alleviate BLM-induced pulmonary fibrosis and TGF-β1-induced HLFs cells damage in mice by inhibiting TGF-β1/smad2/3 signaling pathway.
Keywords/Search Tags:Pirfenidone, Pulmonary fibrosis, TGF-β1, Smad2/3
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