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

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

    Research output: Contribution to journalArticlepeer-review

    8 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)463-467
    Number of pages5
    JournalPhytotherapy Research
    Volume27
    Issue number3
    DOIs
    Publication statusPublished - 2013 Mar

    Keywords

    • alpha smooth muscle actin
    • extracellular matrix
    • mitogen-activated protein kinases
    • myofibroblast
    • nasal polyp
    • transforming growth factor-beta 1

    ASJC Scopus subject areas

    • Pharmacology

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