Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition
DC Field | Value | Language |
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dc.contributor.author | Kyung, Sun Young | - |
dc.contributor.author | Kim, Dae Young | - |
dc.contributor.author | Yoon, Jin Young | - |
dc.contributor.author | Son, Eun Suk | - |
dc.contributor.author | Kim, Yu Jin | - |
dc.contributor.author | Park, Jeong Woong | - |
dc.contributor.author | Jeong, Sung Hwan | - |
dc.date.available | 2020-02-27T11:40:52Z | - |
dc.date.created | 2020-02-07 | - |
dc.date.issued | 2018-04-02 | - |
dc.identifier.issn | 2050-6511 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3860 | - |
dc.description.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)-beta 1-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-beta 1-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-beta 1, E-cadherin (E-cad), and alpha-smooth muscle actin (SMA) in lung tissues. Results: SFN reversed mesenchymal-like changes induced by TGF-beta 1 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 alpha-SMA decreased in A549 cells after SFN treatment. In addition, SFN inhibited TGF-beta 1-induced mRNA expression of the EMT-related transcription factors, Slug, Snail, and Twist. The SFN treatment attenuated TGF-beta 1-induced expression of fibrosis-related proteins, such as fibronection, collagen I, collagen IV, and alpha-SMA in MRC-5 cells. Furthermore, SFN reduced the TGF-beta 1-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-beta 1 expression, and the levels of collagen I in the lungs of mice. Conclusions: SFN showed a significant anti-fibrotic effect in TGF-beta-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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | BMC | - |
dc.relation.isPartOf | BMC PHARMACOLOGY & TOXICOLOGY | - |
dc.subject | CANCER CELLS | - |
dc.subject | BETA | - |
dc.subject | NRF2 | - |
dc.subject | PIRFENIDONE | - |
dc.subject | MECHANISMS | - |
dc.subject | INDUCTION | - |
dc.subject | BLEOMYCIN | - |
dc.subject | PATHWAYS | - |
dc.subject | DISEASE | - |
dc.subject | EMT | - |
dc.title | Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000428887400001 | - |
dc.identifier.doi | 10.1186/s40360-018-0204-7 | - |
dc.identifier.bibliographicCitation | BMC PHARMACOLOGY & TOXICOLOGY, v.19 | - |
dc.identifier.scopusid | 2-s2.0-85044829624 | - |
dc.citation.title | BMC PHARMACOLOGY & TOXICOLOGY | - |
dc.citation.volume | 19 | - |
dc.contributor.affiliatedAuthor | Kyung, Sun Young | - |
dc.contributor.affiliatedAuthor | Kim, Dae Young | - |
dc.contributor.affiliatedAuthor | Yoon, Jin Young | - |
dc.contributor.affiliatedAuthor | Son, Eun Suk | - |
dc.contributor.affiliatedAuthor | Kim, Yu Jin | - |
dc.contributor.affiliatedAuthor | Park, Jeong Woong | - |
dc.contributor.affiliatedAuthor | Jeong, Sung Hwan | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Idiopathic pulmonary fibrosis | - |
dc.subject.keywordAuthor | Bleomycin | - |
dc.subject.keywordAuthor | Sulforaphane | - |
dc.subject.keywordAuthor | Epithelial-mesenchymal transition | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | BETA | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | PIRFENIDONE | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | BLEOMYCIN | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | EMT | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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