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논문 기본 정보

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학술저널
저자정보
Kim, Eun-Jung (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) Choi, In-Seok (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) Yoon, Ji-Young (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) Park, Bong-Soo (Department of Oral Anatomy, School of Dentistry, Pusan National University) Yoon, Ji-Uk (Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University) Kim, Cheul-Hong (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute)
저널정보
대한치과마취과학회 Journal of dental anesthesia and pain medicine Journal of dental anesthesia and pain medicine 제16권 제1호
발행연도
2016.1
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39 - 47 (9page)

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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 $H_2O_2$-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% $CO_2$, 21% $O_2$, and 74% $N_2$) without propofol. Hydrogen peroxide ($H_2O_2$) group cells were exposed to $H_2O_2\;(200{\mu}M)$ for 2 h, propofol preconditioning (PPC)/$H_2O_2$ group cells were pretreated with propofol then exposed to $H_2O_2$, 3-methyladenine (3-MA)/PPC/$H_2O_2$ cells were pretreated with 3-MA (1 mM) and propofol, then were exposed to $H_2O_2$. 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 $H_2O_2$, and this effect was rescued by propofol preconditioning. Propofol preconditioning effectively decreased $H_2O_2$-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-${\beta}1$. Conclusions: This study suggests that propofol preconditioning has a protective effect on $H_2O_2$-induced hFOB cell death, which is mediated by autophagy activation.
#Propofol #Oxidative Stress #Osteoblasts #Autophagy

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참고문헌 (37)

참고문헌 신청
Teitelbaum SL / 2000 / Bone resorption by osteoclasts / Science 289:1504~1508 google schola Boyle WJ / 2003 / Osteoclast differentiation and activation / Nature 423:337~342 google schola Yamaguchi A / 2000 / Regulation of osteoblast differentiation mediated by bone morphogenetic proteins, hedgehogs, and Cbfa1 / Endocr Rev 21:393~411 google schola Wozney JM / 1988 / Novel regulators of bone formation: Molecular clones and activities / Science 242:1528~1534 google schola Xu ZS / 2011 / Hydrogen sulfide protects MC3T3-E1 osteoblastic cells against H2O2-induced oxidative damage-implications for the treatment of osteoporosis / Free Radic Biol Med 50:1314~1323 google schola

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