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Atractylodin Suppre...
Atractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice
- Artikel/kapitelEngelska2021
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LIBRIS-ID:oai:prod.swepub.kib.ki.se:148027510
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http://kipublications.ki.se/Default.aspx?queryparsed=id:148027510URI
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https://doi.org/10.3390/ijms222011152DOI
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Språk:engelska
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Sammanfattning på:engelska
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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.
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Zhang, X
(författare)
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Lin, SC
(författare)
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Lin, YC
(författare)
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Li, CH
(författare)
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Akhrymuk, I
(författare)
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Lin, SH
(författare)
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Lin, CC
(författare)
Sammanhörande titlar
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Ingår i:International journal of molecular sciences: MDPI AG22:201422-0067
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