Wogonin inhibits transforming growth factor beta 1-induced extracellular matrix production via the p38/activator protein 1 signaling pathway in nasal polyp-derived fibroblasts
- Authors
- Ryu, Nam Hyoung; Shin, Jae-Min; Um, Ji-Young; Park, Il-Ho; Lee, Heung-Man
- Issue Date
- 7월-2016
- Publisher
- SAGE PUBLICATIONS INC
- Citation
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY, v.30, no.4, pp.E128 - E133
- Indexed
- SCIE
SCOPUS
- Journal Title
- AMERICAN JOURNAL OF RHINOLOGY & ALLERGY
- Volume
- 30
- Number
- 4
- Start Page
- E128
- End Page
- E133
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/88193
- DOI
- 10.2500/ajra.2016.30.4329
- ISSN
- 1945-8924
- Abstract
- Background: Wogonin has been shown to have antifibrotic and anti-inflammatory effects in the lower airway. The purpose of this study was to evaluate the effects of wogonin on transforming growth factor (TGF) beta 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction, and to determine the molecular mechanisms of wogonin in nasal polyp-derived fibroblasts (NPDF). Methods: NPDFs were isolated from nasal polyps from eight patients. TGF-beta 1-induced NPDFs were treated with wogonin. Cytotoxicity was evaluated by using a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Fibroblast migration was evaluated with transwell and scratch migration assays. The expression levels of beta-smooth muscle actin, fibronectin, phosphorylated-p38, and c-Fos were determined by Western blot and/or reverse transcription-polymerase chain reaction. The total collagen amount was analyzed with the Sircol collagen assay, and contractile activity was measured by a collagen gel contraction assay. Results: Wogonin (0-60 mu M) had no significant cytotoxic effects on TGF-beta 1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of alpha-smooth muscle actin and fibronectin were significantly reduced in wogonin-treated NPDFs. Collagen production and contraction were also significantly decreased by wogonin treatment. Wogonin markedly inhibited activation of the p38/activator protein 1 pathway in TGF-beta 1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-beta 1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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