Catechins reduce inflammation in lipopolysaccharide-stimulated dental pulp cells by inhibiting activation of the NF-κB pathway.

To ascertain the anti-inflammation mechanism of catechins in lipopolysaccharide-treated human dental pulp cells (HDPCs).Expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 was measured using quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assays. The anti-inflammatory mechanism was explored by examining activation of nuclear factor-kappa B (NF-κB) signaling using qPCR, western blotting, and immunofluorescence staining.HDPC proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3-gallate (EGCG). mRNA expression of the pro-inflammatory cytokine TNF-α, IL-1β and IL-6 was decreased significantly in ECG- and EGCG-treated HDPCs. Subsequently, the effects of ECG and EGCG upon activation of NF-κB signaling were evaluated by western blotting and immunofluorescence staining. Expression of p-p65 protein in HDPCs treated with ECG, EGCG or an NF-κB inhibitor (Bay11-7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining.Catechin could reduce lipopolysaccharide-stimulated inflammation in HDPCs by inhibiting activation of the NF-κB pathway.