Effects of propofol-induced autophagy against oxidative stress in human osteoblasts

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(2)O(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(2)O(2)) group cells were exposed to H(2)O(2) (200 µM) for 2 h, propofol preconditioning (PPC)/H(2)O(2) group cells were pretreated with propofol then exposed to H(2)O(2), 3-methyladenine (3-MA)/PPC/H(2)O(2) cells were pretreated with 3-MA (1 mM) and propofol, then were exposed to H(2)O(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(2)O(2), and this effect was rescued by propofol preconditioning. Propofol preconditioning effectively decreased H(2)O(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-β1. CONCLUSIONS: This study suggests that propofol preconditioning has a protective effect on H(2)O(2)-induced hFOB cell death, which is mediated by autophagy activation.