Dexmedetomidine attenuates H2O2-induced cell death in human osteoblasts
윤지영, 박정훈, 김은정, 박봉수, 윤지욱, 신상욱, 김도완,
소속 상세정보
윤지영 ( Yoon Ji-Young ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
박정훈 ( Park Jeong-Hoon ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
김은정 ( Kim Eun-Jung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
박봉수 ( Park Bong-Soo ) - Pusan National University School of Dentistry Department of Oral Anatomy
윤지욱 ( Yoon Ji-Uk ) - Pusan National University School of Medicine Department of Anesthesiology and Pain Medicine
신상욱 ( Shin Sang-Wook ) - Pusan National University School of Medicine Department of Anesthesiology and Pain Medicine
김도완 ( Kim Do-Wan ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
KMID : 0980320160160040295
Abstract
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.
키워드
Dexmedetomidine; Osteoblasts; Oxidative stress
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