The Effects And Mechanism Of Li Tao Kang Xian Fang On Transformation Of Alveolar Type Ⅱ Cells

Objective:Pulmonary fibrosis results from infection,drugs, chemicals,organic or inorganic dust,and other autoimmune diseases,that stimulate alveolar damage.It is a leading cause of Chronic obstructive pulmonary disease,Idiopathic pulmonary fibrosis and other serious lung diseases.As the alveolar epithelial typeⅡcells to mesenchymal cell transformation(EMT) is an important factors of pulmonary fibrosis,so we adopted A549 cells in this experiment and used transforming growth factor induced EMT to occur in A549 cells to study the effect of Li Tao Kang Xian Fang droplet in EMT.Real-time PCR,Western-blot and ELISA was introduced to define the biology basic of Li Tao Kang Xian Fang droplet playing a anti- fibrosis role by controling EMT.Methods:Different concentrations of Li Tao Kang Xian Fang was used to intervene A549 cells in vitro.ELISA were used to show the retative contents of the TGF-β1 in A549 cells.We used TGF-β1 to induce the occurrence of EMT.The collagenⅠand collagenⅢmRNA level was monitored by real-time PCR,the protein level of phosphorylation Erk1/2 were examined by western blot analysis. Cell apoptosis and cell cycle distribution were determined by flow cytometry.The protein level of phosphorylation Erk1/2 were examined by western blot analysis.Results:Our data showed that contents of the TGF-β1 ruduced after 24h intervention of different concentrations of Li Tao Kang Xian Fang.In TGF-β1-induced cells,vimentin espression have a sharp increase but cytokeratina espression have a relative reduction.The level of collagenⅠandⅢshow Significantly higher.By intervening of different concentrations of Li Tao Kang Xian Fang,vimentin espression was significantly lower,yet cytokeratina espression was significantly higher than that in the model group.Meantime,It bring a obvious reduction in espression of collagenⅠ,Ⅲand phosphorylation Erk1/2.Conclusion:Li Tao Kang Xian Fang can drop the EMT rates of TGF-β1 -induced A549 cells,thereby ruduce ACEⅡcells to epithelial cells.It lead to a reduction of lung fibroblast production,to inhibit the occurrence of pulmonary fibrosis,so as to achieve an anti- fibrosis role.The possible mechanism maybe by reducing the transforming growth factor(TGF-β) releasion,interveningⅠandⅢcollagen mRNA expression,and affecting cell phosphorylation Erk1/ 2 expression.