Simvastatin inhibits the expression of inflammatory cytokines and cell adhesion molecules induced by LPS in human dental pulp cells

AimTo investigate the effect of simvastatin on lipopolysaccharide (LPS)-stimulated inflammatory cytokines, cell adhesion molecules and nuclear factor-B (NF-B) transcription factors in human dental pulp cells (HDPCs). MethodologyThe effect of LPS and simvastatin on human dental pulp cell (HDPCs) viability was measured using a 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyltetrazolium bromide (MTT) assay. The expression of inflammatory cytokines and cell adhesion molecules was evaluated by reverse-transcription polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. NF-B transcription factors were evaluated by Western blot analysis. Statistical analysis was performed with analysis of variance (anova). ResultsThe viability of cells exposed to different concentrations of E.coli LPS, P.gingivalis LPS and simvastatin was not significantly different compared with that of control cells (P>0.05). LPS significantly increased interleukin (IL)-1 (P<0.05) and IL-6 mRNA expression (P<0.05) and vascular cell adhesion molecule-1 (VCAM-1) (P<0.05) and intercellular adhesion molecule-1 (ICAM-1) protein expression (P<0.05) in HDPCs. Treatment with simvastatin significantly attenuated LPS-stimulated production of IL-1, IL-6, VCAM-1 and ICAM-1 (P<0.05). Treatment with simvastatin decreased LPS-induced expression of p65 and phosphorylation of IB and also significantly decreased the phosphorylation of p65 and IB in the cytoplasm and the level of p65 in the nucleus (P<0.05). ConclusionsSimvastatin has a suppressing effect on LPS-induced inflammatory cytokine, cell adhesion molecules and NF-B transcription factors in HDPCs. Therefore, simvastatin might be a useful candidate as a pulp-capping agent in vital pulp therapy.