Ji Woong Jung and Il-Ho Park contributed equally to this work.
Naringenin Inhibits Extracellular Matrix Production via Extracellular Signal-Regulated Kinase Pathways in Nasal Polyp-Derived Fibroblasts
Article first published online: 2 JUN 2012
Copyright © 2012 John Wiley & Sons, Ltd.
Volume 27, Issue 3, pages 463–467, March 2013
How to Cite
Jung, J. W., Park, I.-H., Cho, J.-S. and Lee, H.-M. (2013), Naringenin Inhibits Extracellular Matrix Production via Extracellular Signal-Regulated Kinase Pathways in Nasal Polyp-Derived Fibroblasts. Phytother. Res., 27: 463–467. doi: 10.1002/ptr.4735
- Issue published online: 6 MAR 2013
- Article first published online: 2 JUN 2012
- Manuscript Accepted: 20 APR 2012
- Manuscript Revised: 19 APR 2012
- Manuscript Received: 14 FEB 2012
- alpha smooth muscle actin;
- nasal polyp;
- mitogen-activated protein kinases;
- extracellular matrix;
- transforming growth factor-beta 1
Naringenin, a natural predominant flavanone derived from plant food, has antifibrotic activity. The purposes of this study were to determine the effect of naringenin on myofibroblast differentiation and extracellular matrix (ECM) production in nasal polyp-derived fibroblasts (NPDFs) and to determine the molecular mechanism of the effect of naringenin on NPDFs. NPDFs were incubated and treated with transforming growth factor (TGF)-β1. The expression of alpha smooth muscle actin (α-SMA), fibronectin, and collagen type I mRNA was determined by a reverse transcription-polymerase chain reaction, and the expression of those proteins was determined by immunofluorescence staining or Western blotting. Expression of several signaling molecules of the TGF-β1 pathway was evaluated by Western blot analysis. Naringenin inhibits expression of an indicator of myofibroblast differentiation (α-SMA) and ECM production, including collagen type 1 and fibronectin. Naringenin only suppressed the expression of extracellular signal-regulated protein kinase (pERK)1/2 among evaluated signaling molecules. PD98059 (a specific inhibitor of ERK1/2 kinase) also suppressed the increased expression of fibronectin, collagen type I, and α-SMA in TGF-β1-induced NPDFs. These results suggest the possibility that naringenin may play an inhibitory role in the production of the ECM in the development of nasal polyps. Copyright © 2012 John Wiley & Sons, Ltd.