Naringenin inhibits extracellular matrix production via extracellular signal-regulated kinase pathways in nasal polyp-derived fibroblasts.

作者: Ji Woong Jung , Il-Ho Park , Jung-Sun Cho , Heung-Man Lee

DOI: 10.1002/PTR.4735

关键词:

摘要: Naringenin, a natural predominant flavanone derived from plant food, has antifibrotic activity. The purposes of this study were to determine the effect naringenin on myofibroblast differentiation and extracellular matrix (ECM) production in nasal polyp-derived fibroblasts (NPDFs) molecular mechanism NPDFs. NPDFs incubated treated with transforming growth factor (TGF)-β1. expression alpha smooth muscle actin (α-SMA), fibronectin, collagen type I mRNA was determined by reverse transcription-polymerase chain reaction, those proteins immunofluorescence staining or Western blotting. Expression several signaling molecules TGF-β1 pathway evaluated blot analysis. Naringenin inhibits an indicator (α-SMA) ECM production, including 1 fibronectin. only suppressed signal-regulated protein kinase (pERK)1/2 among molecules. PD98059 (a specific inhibitor ERK1/2 kinase) also increased I, α-SMA TGF-β1-induced These results suggest possibility that may play inhibitory role development polyps. Copyright © 2012 John Wiley & Sons, Ltd.

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