ArticleInternational journal of molecular sciences2021
Atractylodin Suppresses TGF-β-Mediated Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells and Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanisms of IL-17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats.Clinical and experimental pharmacology & physiology · 2026Article
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- Atractylodin modulates ASAH3L to improve galactose metabolism and inflammation to alleviate acute lung injury.iScience · 2024Article
- The analysis of boric acid effect on epithelial-mesenchymal transition of CD133 + CD117 + lung cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
- Authenticating the geographic origins ofFrontiers in plant science · 2023Article
- Losartan enhances the suppressive effect of pirfenidone on the bleomycin-induced epithelial-mesenchymal transition and oxidative stress in A549 cell line.Iranian journal of basic medical sciences · 2023Article
- Article
- Atractylodin Induces Apoptosis and Inhibits the Migration of A549 Lung Cancer Cells by Regulating ROS-Mediated Signaling Pathways.Molecules (Basel, Switzerland) · 2022Article
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
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-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.
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