Dexmedetomidine attenuates H2O2-induced cell death in human osteoblasts.

Abstract

BackgroundReactive oxygen species play critical roles in homeostasis and cell signaling. Dexmedetomidine, a specific agonist of the α2-adrenoceptor, has been commonly used for sedation, and it has been reported to have a protective effect against oxidative stress. In this study, we investigated whether dexmedetomidine has a protective effect against H2O2-induced oxidative stress and the mechanism of H2O2-induced cell death in normal human fetal osteoblast (hFOB) cells.MethodsCells were divided into three groups: control group—cells were incubated in normoxia without dexmedetomidine, hydrogen peroxide (H2O2) group—cells were exposed to H2O2 (200 µM) for 2 h, and Dex/H2O2 group—cells were pretreated with dexmedetomidine (5 µM) for 2 h then exposed to H2O2 (200 µM) for 2 h. Cell viability and apoptosis were evaluated. Osteoblast maturation was determined by assaying bone nodular mineralization. Expression levels of bone-related proteins were determined by western blot.ResultsCell viability was significantly decreased in the H2O2 group compared with the control group, and this effect was improved by dexmedetomidine. The Hoechst 33342 and Annexin-V FITC/PI staining revealed that dexmedetomidine effectively decreased H2O2-induced hFOB cell apoptosis. Dexmedetomidine enhanced the mineralization of hFOB cells when compared to the H2O2 group. In western blot analysis, bone-related protein was increased in the Dex/H2O2 group.ConclusionsWe demonstrated the potential therapeutic value of dexmedetomidine in H2O2-induced oxidative stress by inhibiting apoptosis and enhancing osteoblast activity. Additionally, the current investigation could be evidence to support the antioxidant potential of dexmedetomidine in vitro.