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Oncol Rep ; 31(5): 2422-8, 2014 May.
Article in English | MEDLINE | ID: mdl-24647969

ABSTRACT

Oral submucous fibrosis (OSF) is a chronic inflammatory disease characterized by the accumulation of excess collagen, and areca nut chewing has been proposed as a significant etiological factor for disease manifestation. However, the underlying molecular mechanisms regarding areca nut chewing-induced OSF are only partially understood. Herein, we reported that arecoline markedly induced morphologic change in HaCaT epithelial cells, but had no obvious effect on Hel fibroblast cells. MTS assay revealed that arecoline significantly suppressed HaCaT cell viability. Moreover, flow cytometric analysis indicated that arecoline substantially promoted HaCaT cell, but not Hel cell apoptosis in a dose-dependent manner. Furthermore, arecoline-induced HaCaT cell apoptosis was found to be associated with increased expression and activation of cleaved-Bid, cleaved-PARA and cleaved-caspase-3. Collectively, our results suggest that HaCaT epithelial cells are more sensitive than Hel fibroblast cells to arecoline-induced cytotoxicity, which may be involved in the pathogenesis of OSF.


Subject(s)
Apoptosis/drug effects , Arecoline/pharmacology , Fibroblasts/drug effects , Keratinocytes/drug effects , Oral Submucous Fibrosis/pathology , Areca/adverse effects , BH3 Interacting Domain Death Agonist Protein/metabolism , Caspase 3/metabolism , Cell Line , Cell Proliferation , Cholinergic Agonists/pharmacology , Epithelial Cells/drug effects , Feeding Behavior , Fibroblasts/cytology , Humans , Keratinocytes/cytology , Mouth Mucosa/pathology , Oral Submucous Fibrosis/chemically induced
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