摘要
Abstract
Objective:To investigate the effect and mechanism of carvacrol(CVL)on paraquat-induced pulmonary fibrosis(PF)in mice.Methods:Thirty-six mice were randomly divided into blank group(NS),model group(PQ),carvacrol low-dose group(CVL 10 mg/kg),carvacrol high-dose group(CVL 20 mg/kg),with nine in each group.Modeling of paraquat(20 mg/kg)by intraperitoneal injection,from the second day of model making,the treatment groups received intraperitoneal injection with carvacrol every day for 21 days.Lung histopathological changes and collagen fiber deposition were observed by HE and Masson staining.Serum and lung tissue hydroxyproline levels were measured using a hydroxyproline kit.The TNF-α,IL-1β and IL-6 in the lung tissue were determined by ELISA.The expressions of α-SMA,E-cadherin,TGF-β1 and Smad2/3 in mouse lung tissues were detected by IHC.Expressions of Collagen1,α-SMA,E-cadherin,TGF-β1 protein,Smad2/3 protein and p-Smad 2/3 protein in lung tissue were detected by Western blot.TGF-β1 gene expression was determined by RT-PCR.Results:Compared with model group,after carvacrol treat-ment,inflammation in lung tissue of mice and collagen fiber deposition were decreased.The concentrations of TNF-α,IL-1β and IL-6 in the lung tissue were decreased(P<0.05).The expressions of the proteins including the Collagen1,α-SMA and TGF-β1/Smad sig-naling pathway was reduced(P<0.05).The E-cadherin expression was upregulated(P<0.05).The mRNA level of TGF-β1 was also downregulated(P<0.05).Conclusion:Carvacrol ameliorated pulmonary fibrosis in paraquat-induced mice.The mechanism may be re-lated to the downregulation of TGF-β1/Smad signaling to prevent epithelial-mesenchymal transition(EMT)and the suppression of in-flammation.关键词
香芹酚/肺纤维化/百草枯/炎症因子/TGF-β1/Smad信号通路/上皮-间质转化Key words
Carvacrol/Pulmonary fibrosis/Paraquat/Inflammatory factors/TGF-β1/Smad signaling pathway/Epithelial-mes-enchymal transition分类
医药卫生
