IADR Abstract Archives
Effect of Simvastatin on the Regulation of Inflammatory Cytokine in the Dental Pulp Cells
Objectives: Simvastatin, a hydroxy-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, was first introduced in 1988. Simvastatin have been used to reduce the risk of cardiovascular disease. Simvastatin produce a reduction of low-density lipoprotein cholesterol (LDL-C) and with excellent tolerability and very little risk of adverse effect
It was reported that simvastatin can promotes osteoblast differentiation and mineralization in MC3T3-E1 cells, and promotes odontoblast differentiation in human dental pulp cells.
In addition, simvastatin also have an anti-inflammatory effect. Simvastatin prevents inflammatory process induced by lipopolysaccharide and atorvastatin reduces the inflammation through the inhibition of NF-kappaB activity
The purpose of this study is to reveal the effect of simvastatin to suppress the inflammatory cytokine expression in the dental pulp cells and their possible mechanism
Methods: Human dental pulp cells were cultured in the DMEM with 10% FBS and 1% antibiotics. MTT assay was performed to evaluate cytotoxicity of simbastatin. E. coli LPS and P.g LPS was treated to induce inflammatory cytokine. RT-PCR, ELISA and Western blot were performed to evaluate anti-inflammatory effect of simbastatin and possible mechanism.
All experiments were performed in triplicate. Each value represents the mean± SD. Statistical significance was determined using Student’s t-test when compared with control. Differences with P-values <0.05 were considered significant.
Results: The cell viability exposed to different concentration of E.coli LPS, Porphyromonas gingivalis LPS, and simvastatin was not significantly different compared to control.
E.coli LPS and P.g LPS increased IL-1β and IL-6 mRNA expression and VCAM-1 and ICAM-1 expression.
Treatment of simvastatin effectively inhibited IL-1β and IL-6 expression in LPS stimulated HDPCs.
Upregulated VCAM-1, ICAM-1 production in HDPCs stimulated with LPS was inhibited by the simvastatin treatment.
Simbastatin decreased NF-kB (p65) expression which was induced by LPS.
Conclusions: In this study, simbastatin decreased inflammatory cytokine expression in the dental pulp cells and simbastatin mediated reduction of inflammatory cytokine is thought to be the result of the inhibition of the NF-kB pathway.
It was reported that simvastatin can promotes osteoblast differentiation and mineralization in MC3T3-E1 cells, and promotes odontoblast differentiation in human dental pulp cells.
In addition, simvastatin also have an anti-inflammatory effect. Simvastatin prevents inflammatory process induced by lipopolysaccharide and atorvastatin reduces the inflammation through the inhibition of NF-kappaB activity
The purpose of this study is to reveal the effect of simvastatin to suppress the inflammatory cytokine expression in the dental pulp cells and their possible mechanism
Methods: Human dental pulp cells were cultured in the DMEM with 10% FBS and 1% antibiotics. MTT assay was performed to evaluate cytotoxicity of simbastatin. E. coli LPS and P.g LPS was treated to induce inflammatory cytokine. RT-PCR, ELISA and Western blot were performed to evaluate anti-inflammatory effect of simbastatin and possible mechanism.
All experiments were performed in triplicate. Each value represents the mean± SD. Statistical significance was determined using Student’s t-test when compared with control. Differences with P-values <0.05 were considered significant.
Results: The cell viability exposed to different concentration of E.coli LPS, Porphyromonas gingivalis LPS, and simvastatin was not significantly different compared to control.
E.coli LPS and P.g LPS increased IL-1β and IL-6 mRNA expression and VCAM-1 and ICAM-1 expression.
Treatment of simvastatin effectively inhibited IL-1β and IL-6 expression in LPS stimulated HDPCs.
Upregulated VCAM-1, ICAM-1 production in HDPCs stimulated with LPS was inhibited by the simvastatin treatment.
Simbastatin decreased NF-kB (p65) expression which was induced by LPS.
Conclusions: In this study, simbastatin decreased inflammatory cytokine expression in the dental pulp cells and simbastatin mediated reduction of inflammatory cytokine is thought to be the result of the inhibition of the NF-kB pathway.