Abstract:
:Amiodarone is a high effectiveness anti-arrhythmia agent which is able to induce pulmonary fibrosis. Many studies have shown that the epithelial-mesenchymal transition (EMT) was a significant process in pulmonary fibrosis. So far, there are no studies about whether EMT was associated with amiodarone-induced pulmonary fibrosis, which was therefore explored in this study. In addition, the underlying mechanisms of amiodarone-induced pulmonary fibrosis were examined in vitro. We found the EMT marker (α-SMA) was significantly increased, while the E-cadherin was significantly decreased in adenocarcinomic human alveolar basal epithelial cells (A549) after amiodarone treatment, suggesting that the epithelial cells were an important source of mesenchymal cells. Transforming growth factor beta1 (TGF-β1) was also increased significantly after amiodarone treatment. In conclusion, this study suggested amiodarone could induce pulmonary fibrosis via EMT, and the TGF-β1 may be a key profibrotic cytokine in mechanisms of amiodarone-induced pulmonary fibrosis.
journal_name
Drug Chem Toxicoljournal_title
Drug and chemical toxicologyauthors
Weng J,Chen H,Wu H,Tu M,Wang Z,Chen D,Wang Z,Chen Cdoi
10.1080/01480545.2018.1497055subject
Has Abstractpub_date
2020-07-01 00:00:00pages
415-422issue
4eissn
0148-0545issn
1525-6014journal_volume
43pub_type
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