|Title:||Atractylodin Suppresses TGF-beta-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice||Authors:||Chang, Kai-Wei
|Keywords:||TRANSCRIPTION FACTOR SNAIL;E-CADHERIN;EXTRACELLULAR-MATRIX;EXPRESSION;INFLAMMATION||Issue Date:||Oct-2021||Publisher:||MDPI||Journal Volume:||22||Journal Issue:||20||Source:||INT J MOL SCI||Abstract:||
Idiopathic 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-beta 1)-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-beta 1 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-beta 1-induced EMT in A549 cells and bleomycin-induced pulmonary fibrosis in mice.
|Appears in Collections:||海洋生物科技學士學位學程(系)|
03 GOOD HEALTH AND WELL-BEING
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