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

Aim: To ascertain the anti‐inflammation mechanism of catechins in lipopolysaccharide‐treated human dental pulp cells (HDPCs). Methods: 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. Results: Human dental pulp cells proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3‐gallate (EGCG). mRNA expression of the pro‐inflammatory cytokines 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 (Bay 11‐7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining. Conclusions: Catechin could reduce lipopolysaccharide‐stimulated inflammation in HDPCs by inhibiting activation of the NF‐κB pathway. [ABSTRACT FROM AUTHOR]