Wogonin inhibits transforming growth factor 1-induced extracellular matrix production via the p38/activator protein 1 signaling pathway in nasal polyp-derived fibroblasts

Nam Hyoung Ryu, Jae Min Shin, Ji Young Um, Il Ho Park, Heung Man Lee

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

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) 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-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 -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 M) had no significant cytotoxic effects on TGF-1-induced NPDFs. Migration of NPDFs was significantly inhibited by wogonin treatment. The expression levels of -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-1-induced NPDFs. Conclusion: These results indicated that wogonin may inhibit TGF-1-induced myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction through the p38/activator protein-1 pathway in NPDFs.

Original languageEnglish
Pages (from-to)e128-e133
JournalAmerican Journal of Rhinology and Allergy
Volume30
Issue number4
DOIs
Publication statusPublished - 2016 Jul 1

Bibliographical note

Funding Information:
This study was supported by a grant from the Korean Health Technology RandD Project, Ministry of Health and Welfare, Republic of Korea (HI15C1512). Also, it was supported by the Basic Science Research Program through the National Research Foundation of Korea, which is funded by the Ministry of Education (2013R1A1A2059716)

Publisher Copyright:
Copyright © 2016, OceanSide Publications, Inc., U.S.A.

ASJC Scopus subject areas

  • Immunology and Allergy
  • Otorhinolaryngology

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