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.

AIM: 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.