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Arecoline stimulated early growth response‐1 production in human buccal fibroblasts: Suppression by epigallocatechin‐3‐gallate
Author(s) -
Hsieh YuPing,
Chen HsinMing,
Chang Jenny ZweiChieng,
Chiang ChunPin,
Deng YiTing,
Kuo Mark YenPing
Publication year - 2015
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.23614
Subject(s) - arecoline , oral submucous fibrosis , areca , western blot , chemistry , microbiology and biotechnology , fibroblast , signal transduction , gallate , buccal administration , cancer research , pharmacology , biochemistry , biology , medicine , nut , gene , receptor , muscarinic acetylcholine receptor , structural engineering , engineering , in vitro
Background Early growth response‐1 (Egr‐1) protein plays an important role in many human fibrotic diseases. Areca nut chewing is the most important risk factor of oral submucous fibrosis (OSF). Methods Egr‐1 protein expression in OSF was examined using antibody to Egr‐1. Arecoline‐induced Egr‐1 expression and its signaling pathways were assessed by Western blot analyses in human buccal mucosal fibroblasts (BMFs). Results Elevated Egr‐1 staining was observed in epithelial cells, fibroblast, and inflammatory cells in 7 of 10 OSF cases. Arecoline, a main alkaloid found in the areca nut, stimulated Egr‐1 synthesis in BMFs. Pretreatment with antioxidant N‐acetyl‐L‐cysteine, c‐Jun NH2‐terminal kinase inhibitor SP600125, and extracellular signal‐regulated kinase inhibitor PD98059 significantly reduced arecoline‐induced Egr‐1 synthesis. Epigallocatechin‐3‐gallate (EGCG) inhibited arecoline‐induced Egr‐1 synthesis and collagen gel contraction in a dose‐responsive manner. Conclusion Constitutive Egr‐1 expression during areca nut chewing may play a role in the pathogenesis of OSF. EGCG could be a good candidate for prevention or treatment of OSF. © 2014 Wiley Periodicals, Inc. Head Neck 37 : 493–497, 2015