International journal of molecular sciences, 2021-10, Vol.22 (20), p.11152
2021
Details
- Autor(en) / Beteiligte
- Titel
- Atractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice
- Ist Teil von
- International journal of molecular sciences, 2021-10, Vol.22 (20), p.11152
- Ort / Verlag
- Switzerland: MDPI AG
- Erscheinungsjahr
- 2021
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- 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-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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1422-0067, 1661-6596eISSN: 1422-0067DOI: 10.3390/ijms222011152Titel-ID: cdi_doaj_primary_oai_doaj_org_article_719e6204cb1648cf9a6fc17c86941541
- Format
- –
- Schlagworte
- A549 Cells, Alveolar Epithelial Cells - drug effects, Alveolar Epithelial Cells - physiology, Alveoli, Animals, atractylodin, Attenuation, Bleomycin, Bleomycin - adverse effects, Collagen, Collagens, Cytokines, Cytotoxicity, Deposition, Down-Regulation - drug effects, Down-Regulation - genetics, E-cadherin, Epithelial cells, epithelial-mesenchymal transition, Epithelial-Mesenchymal Transition - drug effects, Epithelial-Mesenchymal Transition - genetics, Epithelium, Fibroblasts, Fibrosis, Furans - pharmacology, Furans - therapeutic use, Gene expression, Growth factors, Herbal medicine, Humans, idiopathic pulmonary fibrosis, Idiopathic Pulmonary Fibrosis - chemically induced, Idiopathic Pulmonary Fibrosis - genetics, Idiopathic Pulmonary Fibrosis - pathology, Idiopathic Pulmonary Fibrosis - prevention & control, Kinases, Lung diseases, Lungs, Male, MAP kinase, MAPK, Medical prognosis, Medicin och hälsovetenskap, Mesenchyme, Mice, Mice, Inbred C57BL, Pathogenesis, Phosphorylation, Protein kinase, Pulmonary fibrosis, Pulmonary functions, Respiratory function, Signal Transduction - drug effects, Signal Transduction - genetics, Smad2 protein, Smad2/3, Therapeutic targets, Transcription factors, Transforming Growth Factor beta - genetics, Transforming Growth Factor beta - physiology, Transforming growth factor-b1, transforming growth factor-beta 1