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KMID : 0980320160160040295
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Journal of Dental Anesthesia and Pain Medicine
2016 Volume.16 No. 4 p.295 ~ p.302
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Dexmedetomidine attenuates H2O2-induced cell death in human osteoblasts
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Yoon Ji-Young
Park Jeong-Hoon
Kim Eun-Jung
Park Bong-Soo
Yoon Ji-Uk
Shin Sang-Wook
Kim Do-Wan
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Abstract
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Background: Reactive 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.
Methods: Cells 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.
Results: Cell 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.
Conclusions: We 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.
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KEYWORD
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Dexmedetomidine, Osteoblasts, Oxidative stress
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