Study on mechanism of astragaloside Ⅳ in treatment of pulmonary fibrosis with epithelial-mesenchymal transition

OBJECTIVE Currently discussing the clinical treatment of pulmonary fibrosis commonly used drugs astragalus main active ingredient astragalosideⅣ(ASTⅣ) in vitro after transforming growth factor-β1 induced lung adenocarcinoma A549 epithelial cells after epithelial cell interstitial EpithelialMesenchymal Transition(EMT).METHODS The effect of astragalosideIV on the proliferation of A549 cells was detected by MTT assay for the first time.No significant effect of astragaloside on the prolifera.tion of A549 cells was found in the range of 1.25-20 μmol/L.A549 cells in vitro were divided into 5 groups:normal group,control group,low,medium and high experimental groups,which were treated for 72 hours,and the morphological changes of cells in each group were observed by light microscope.Real-time quantitative PCR(qPCR) and Western blotting were performed.Detection of gene and protein expression levels.RESULTS The results of real-time fluorescence quantitative PCR showed that the quantitative analysis of high-dose astragalosideⅣ in the experimental group was lower than that of the control group in the α-SMA analysis,and the difference was statistically significant(P<0.05).The dose of Astragaloside Ⅳ in the experimental group was higher than that of the control group in the E-Cad analysis,and the difference was statistically significant(P<0.05).Western Blot results showed that the expression of α-SMA antibody in the high-dose and low-dose experimental group was lower than that in the control group,the difference was statistically significant(P<0.05).The high-dose experimental group had a significantly higher expression of E-Cad antibody than the control group,the difference was statistically significant(P<0.01).CONCLUSION This study uses A549 epithelial cells as a model,A549 cells were modeled and confirmed that Astragaloside can effectively inhibit TGF-β1-induced epithelialmesenchymal transition(EMT) and provide a new basis for the treatment of pulmonary fibrosis.

OBJECTIVE Currently discussing the clinical treatment of pulmonary fibrosis commonly used drugs astragalus main active ingredient astragalosideⅣ （ASTⅣ） in vitro after transforming growth factor-β1 induced lung adenocarcinoma A549 epithelial cells after epithelial cell interstitial Epithelial- Mesenchymal Transition（EMT）. METHODS The effect of astragalosidelV on the proliferation of A549 cells was detected by MTT assay for the first time. No significant effect of astragaloside on the proliferation of A549 cells was found in the range of 1.25-20 μmol/L. A549 cells in vitro were divided into 5 groups： normal group, control group, low, medium and high experimental groups, which were treated for 72 hours, and the morphological changes of cells in each group were observed by light microscope. Real-time quantitative PCR （qPCR） and Western blotting were performed. Detection of gene and protein expression levels. RESULTS The results of real-time fluorescence quantitative PCR showed that the quantitative analysis of high-dose astragalosidelV in the experimental group was lower than that of the control group in the α-SMA analysis, and the difference was statistically significant （P〈0.05）. The dose of Astragaloside IV in the experimental group was higher than that of the control group in the E-Cad analysis, and the difference was statistically significant （P〈0.05）. Western Blot results showed that the expression of cx-SMA antibody in the high-dose and low-dose experimental group was lower than that in the control group, the difference was statistically significant （P〈0.05）. The high-dose experimental group had a significantly higher expression of E-Cad antibody than the control group, the difference was statistically significant （P〈0.01）. CONCLUSION This study uses A549 epithelial cells as a model, A549 cells were modeled and confirmed that Astragaloside can effectively inhibit TGF-β1-induced epithelialmesenchymal transition （EMT） and provide a new basis for the treatment of pulmonary fibrosis.