Atractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

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dc.contributor.authorChang, Kai-Weien
dc.contributor.authorZhang, Xiangen
dc.contributor.authorLin, Shih-Chaoen
dc.contributor.authorLin, Yu-Chaoen
dc.contributor.authorLi, Chia-Hsiangen
dc.contributor.authorAkhrymuk, Ivan V.en
dc.contributor.authorLin, Sheng-Haoen
dc.contributor.authorLin, Chi-Chienen
dc.date.accessioned2021-10-22T14:13:26Zen
dc.date.available2021-10-22T14:13:26Zen
dc.date.issued2021-10-15en
dc.date.updated2021-10-22T13:56:04Zen
dc.description.abstractIdiopathic 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.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationChang, 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.en
dc.identifier.doihttps://doi.org/10.3390/ijms222011152en
dc.identifier.urihttp://hdl.handle.net/10919/105639en
dc.language.isoenen
dc.publisherMDPIen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectidiopathic pulmonary fibrosisen
dc.subjecttransforming growth factor-beta 1en
dc.subjectepithelial-mesenchymal transitionen
dc.subjectatractylodinen
dc.subjectSmad2/3en
dc.subjectMAPKen
dc.titleAtractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Miceen
dc.title.serialInternational Journal of Molecular Scienceen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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