Neutralizing effect of green tea epigallocatechin-3-gallate on nicotine-induced toxicity and chemokine (C-C motif) ligand 5 secretion in human oral epithelial cells and fibroblasts.
Λέξεις-κλειδιά
Αφηρημένη
OBJECTIVE
Tobacco use has been identified as the most important environmental risk factor for periodontitis. The aim of this study was to investigate the effect of green tea epigallocatechin-3-gallate on the nicotine-induced toxic and inflammatory responses in oral epithelial cells and gingival fibroblasts.
METHODS
The effect of nicotine, alone and in combination with the lipopolysaccharide of Aggregatibacter actinomycetemcomitans, on the viability of oral epithelial cells and fibroblasts was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide colorimetric assay. The ability of epigallocatechin-3-gallate to neutralize the nicotine-induced cytotoxicity was then investigated. The nicotine-induced cytokine secretion in epithelial cells and the inhibitory effect of epigallocatechin-3-gallate were determined by enzyme-linked immunosorbent assay.
RESULTS
Our results indicated that nicotine caused a dose-dependent loss of viability in both epithelial cells and fibroblasts. A mixture of nicotine and A. actinomycetemcomitans lipopolysaccharide demonstrated additive instead of synergistic effects on loss of cell viability. Pretreatment of cells with epigallocatechin-3-gallate efficiently neutralized the nicotine-induced toxic effects in epithelial cells and fibroblasts. It also dose dependently inhibited the nicotine-induced secretion of chemokine (C-C motif) ligand 5 by epithelial cells.
CONCLUSIONS
The present study suggests that epigallocatechin-3-gallate, the major polyphenol in green tea, may represent a novel preventive/therapeutic agent for smoking-related periodontitis.
