Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition
Kyung SY, Kim DY, Yoon JY, Son ES, Kim YJ, Park JW, Jeong SH
BMC pharmacology & toxicology · 92 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- University or hospital
- Gachon University
- University or hospital
- Gil Medical Center, Gachon University
- University or hospital
- Gachon University Gil Medical Center
- Grants
- Gil Medical Center, Gachon University (2013-34)
Based on 3 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2018-04-02 · BMC Pharmacol Toxicol · vol. 19 · issue 1 · p. 13
- Publisher
- BioMed Central
- Cited
- 104 citations · more than 97% of similar papers · 5.7× the field average
- Impact
- Top 10% most cited in its field
- References
- 35 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis · Genomics, phytochemicals, and oxidative stress · IL-33, ST2, and ILC Pathways
- Keywords
- Epithelial–mesenchymal transition, Sulforaphane, Pulmonary fibrosis, Transition (genetics), Mesenchymal stem cell, Cancer research, Fibrosis, Cell biology, Chemistry, Medicine, Biology, Pathology, Biochemistry, Gene
- MeSH
- lung, cell line, animals, mice, inbred c57bl, humans, pulmonary fibrosis, isothiocyanates, sulfoxides, collagen type i, bleomycin, transforming growth factor beta, collagen type iv, male, smad2 protein, smad3 protein, epithelial-mesenchymal transition
7 authors
From KR
- Sun Young KyungGachon University; Gachon University Gil Medical Center
- Dae Young KimGachon University
- Jin Young YoonGachon University; Gachon University Gil Medical Center
- Eun Suk SonGachon University; Gachon University Gil Medical Center
- Yu Jin KimGachon University; Gachon University Gil Medical Center
- Jeong Woong ParkGachon University; Gachon University Gil Medical Center
Abstract
Background
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease with no effective treatment. The epithelial-mesenchymal transition (EMT) is a critical stage during the development of fibrosis. To assess the effect of sulforaphane (SFN) on the EMT and fibrosis using an in vitro transforming growth factor (TGF)-β1-induced model and an in vivo bleomycin (BLM)-induced model.
Methods
In vitro studies, cell viability, and cytotoxicity were measured using a Cell Counting Kit-8. The functional TGF-β1-induced EMT and fibrosis were assessed using western blotting and a quantitative real-time polymerase chain reaction. The lungs were analyzed histopathologically in vivo using hematoxylin and eosin and Masson's trichrome staining. The BLM-induced fibrosis was characterized by western blotting and immunohistochemical analyses for fibronectin, TGF-β1, E-cadherin (E-cad), and α-smooth muscle actin (SMA) in lung tissues.
Results
SFN reversed mesenchymal-like changes induced by TGF-β1 and restored cells to their epithelial-like morphology. The results confirmed that the expression of the epithelial marker, E-cadherin, increased after SFN treatment, while expression of the mesenchymal markers, N-cadherin, vimentin, and α-SMA decreased in A549 cells after SFN treatment. In addition, SFN inhibited TGF-β1-induced mRNA expression of the EMT-related transcription factors, Slug, Snail, and Twist. The SFN treatment attenuated TGF-β1-induced expression of fibrosis-related proteins, such as fibronection, collagen I, collagen IV, and α-SMA in MRC-5 cells. Furthermore, SFN reduced the TGF-β1-induced phosphorylation of SMAD2/3 protein in A549 cells and MRC-5 cells. BLM induced fibrosis in mouse lungs that was also attenuated by SFN treatment, and SFN treatment decreased BLM-induced fibronectin expression, TGF-β1 expression, and the levels of collagen I in the lungs of mice.
Conclusions
SFN showed a significant anti-fibrotic effect in TGF-β-treated cell lines and BLM-induced fibrosis in mice. These findings showed that SFN has anti-fibrotic activity that may be considered in the treatment of IPF.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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