Abstract: Objective To elucidate the anti-inflammatory and anti-oxidative properties of resveratrol (RSV) on Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide- (LPS- ) induced human gingival fibroblasts (HGFs). Methods HGF cells were divided into experiment 1 and experiment 2. Cells in experiment 1 were divided into the control group, the LPS group, the RSV 20 μmol/L group, the RSV 40 μmol/L group, the RSV 80 μmol/L group and the LPS+RSV 20 μmol/L group. The cells in experiment 2 were divided into the control group, the LPS group, the LPS+RSV 40 μmol/L group, the LPS+RSV 40 μmol/L+E5564 group and the LPS+E5564 group. Cell viability was evaluated by cell-counting kit-8 assay. IL-1β, IL-6, IL-8, TNF-α, SOD, MDA, and GSH-Px levels were measured by ELISA. Protein expressions were measured by Western blot analysis. Results It was found that 20, 40 and 80 μmol/L RSV had no significant effects on the viability of HGF cells. In LPSinduced HGFs, 40 and 80 μmol/L RSV significantly reduced inflammation by the down-regulation of IL-1β, IL-6, IL-8, and TNF- α expression. And 40 and 80 μmol/L RSV also decreased MDA expression, accompanied by an increase of SOD production (P＜0.05). Meanwhile, 80 μmol/L RSV significantly increased GSH-Px levels (P＜0.05). Additionally, 20, 40 and 80 μmol/L RSV induced deactivation of TLR4/MyD88/NF- κB signaling pathway (P＜0.05). It was found that TLR4 inhibitor (E5564) could further strengthen RSV-reduced inflammation and OS injury by the down-regulation of IL-1β, IL-6, IL-8, and TNF- α production and up-regulation of GSH-Px in LPS-induced HGFs (P＜0.05). Conclusion Resveratrol attenuates the inflammation and OS injury of P. gingivalis LPS-treated HGFs by deactivating TLR4/MyD88/NF-κB signaling pathway.

Key words: veratrum nigrum, alcohols, signal transduction, NF-kappa B, chronic periodontitis, fibroblasts, resveratrol