Dexmedetomidine and LPS co-treatment attenuates inflammatory response on WISH cells via inhibition of p38/NF-kB signaling pathway

ABSTRACT

Background@#Inflammatory dental diseases that occur during pregnancy can cause preterm labor and/or intrauterine growth restriction. Therefore, proactive treatment of dental diseases is necessary during pregnancy. Dexmedetomidine (DEX) is a widely used sedative in the dental field, but research on the effect of DEX on pregnancy is currently insufficient. In this study, we investigated the effects of co-treatment with DEX and lipopolysaccharide (LPS) on inflammatory responses in human amnion-derived WISH cells. @*Methods@#Human amnion-derived WISH cells were treated with 0.001, 0.01, 0.1, and 1 μg/mL DEX with 1 μg/mL LPS for 24 h. Cytotoxicity of WISH cells was evaluated by 3-(4,5-)-2,5-diphenyltetrazolium bromide (MTT) assay. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E 2 (PGE 2 ), p38, and nuclear factor kappa B (NF-κB) was examined by western blot analysis. The mRNA expression of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α was analyzed by real-time quantitative polymerase chain reaction. @*Results@#Co-treatment with DEX and LPS showed no cytotoxicity in the WISH cells. The mRNA expression of IL-1β and TNF-α decreased after co-treatment with DEX and LPS. DEX and LPS co-treatment decreased the protein expression of COX-2, PGE 2 , phospho-p38, and phospho-NF-κB in WISH cells. @*Conclusion@#Co-treatment with DEX and LPS suppressed the expression of COX-2 and PGE 2 , as well as pro-inflammatory cytokines such as IL-1β and TNF-α in WISH cells. In addition, the anti-inflammatory effect of DEX and LPS co-treatment was mediated by the inhibition of p38/NF-κB activation.