Effects of propofol-induced autophagy against oxidative stress in human osteoblasts.
10.17245/jdapm.2016.16.1.39
- Author:
Eun Jung KIM
1
;
In Seok CHOI
;
Ji Young YOON
;
Bong Soo PARK
;
Ji Uk YOON
;
Cheul Hong KIM
Author Information
1. Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Gyeongnam, Korea. anekch@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Propofol;
Oxidative Stress;
Osteoblasts;
Autophagy
- MeSH:
Aging;
Antioxidants;
Apoptosis;
Autophagy*;
Blotting, Western;
Bone Diseases;
Bone Remodeling;
Cell Death;
Cell Line;
Cell Survival;
Collagen Type I;
Fractures, Bone;
Humans*;
Hydrogen Peroxide;
Miners;
Osteoblasts*;
Osteoporosis;
Oxidative Stress*;
Propofol
- From:Journal of Dental Anesthesia and Pain Medicine
2016;16(1):39-47
- CountryRepublic of Korea
- Language:English
-
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.
