Chang, Kai-WeiZhang, XiangLin, Shih-ChaoLin, Yu-ChaoLi, Chia-HsiangAkhrymuk, Ivan V.Lin, Sheng-HaoLin, Chi-Chien2021-10-222021-10-222021-10-15Chang, K.-W.; Zhang, X.; Lin, S.-C.; Lin, Y.-C.; Li, C.-H.; Akhrymuk, I.; Lin, S.-H.; Lin, C.-C. Atractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice. Int. J. Mol. Sci. 2021, 22, 11152.http://hdl.handle.net/10919/105639Idiopathic pulmonary fibrosis (IPF) is characterized by fibrotic change in alveolar epithelial cells and leads to the irreversible deterioration of pulmonary function. Transforming growth factor-beta 1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in type 2 lung epithelial cells contributes to excessive collagen deposition and plays an important role in IPF. Atractylodin (ATL) is a kind of herbal medicine that has been proven to protect intestinal inflammation and attenuate acute lung injury. Our study aimed to determine whether EMT played a crucial role in the pathogenesis of pulmonary fibrosis and whether EMT can be utilized as a therapeutic target by ATL treatment to mitigate IPF. To address this topic, we took two steps to investigate: 1. Utilization of anin vitro EMT model by treating alveolar epithelial cells (A549 cells) with TGF-β1 followed by ATL treatment for elucidating the underlying pathways, including Smad2/3 hyperphosphorylation, mitogen-activated protein kinase (MAPK) pathway overexpression, Snail and Slug upregulation, and loss of E-cadherin. Utilization of an in vivo lung injury model by treating bleomycin on mice followed by ATL treatment to demonstrate the therapeutic effectiveness, such as, less collagen deposition and lower E-cadherin expression. In conclusion, ATL attenuates TGF-β1-induced EMT in A549 cells and bleomycin-induced pulmonary fibrosis in mice.application/pdfenCreative Commons Attribution 4.0 InternationalArticle - Refereed2021-10-22https://doi.org/10.3390/ijms222011152