Effects of propofol-induced autophagy against oxidative stress in human osteoblasts
김은정, 최인석, 윤지영, 박봉수, 윤지욱, 김철홍,
소속 상세정보
김은정 ( Kim Eun-Jung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
최인석 ( Choi In-Seok ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
윤지영 ( Yoon Ji-Young ) - 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
김철홍 ( Kim Cheul-Hong ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
KMID : 0980320160160010039
Abstract
Background: Oxidative stress occurs during the aging process and other conditions such as bone fracture, bone diseases, and osteoporosis, but the role of oxidative stress in bone remodeling is unknown. Propofol exerts antioxidant effects, but the mechanisms of propofol preconditioning on oxidative stress have not been fully explained. Therefore, the aim of this study was to evaluate the protective effects of propofol against H2O2-induced oxidative stress on a human fetal osteoblast (hFOB) cell line via activation of autophagy.
Methods: Cells were randomly divided into the following groups: control cells were incubated in normoxia (5% CO2, 21% O2, and 74% N2) without propofol. Hydrogen peroxide (H2O2) group cells were exposed to H2O2 (200 μM) for 2 h, propofol preconditioning (PPC)/H2O2 group cells were pretreated with propofol then exposed to H2O2, 3-methyladenine (3-MA)/PPC/H2O2 cells were pretreated with 3-MA (1 mM) and propofol, then were exposed to H2O2. 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 and bone nodular mineralization were decreased significantly by H2O2, and this effect was rescued by propofol preconditioning. Propofol preconditioning effectively decreased H2O2-induced hFOB cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol. In western blot analysis, propofol preconditioning increased protein levels of collagen type I, BMP-2, osterix, and TGF-β1.
Conclusions: This study suggests that propofol preconditioning has a protective effect on H2O2-induced hFOB cell death, which is mediated by autophagy activation.
키워드
Propofol; Oxidative Stress; Osteoblasts; Autophagy
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