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Aims: Bone injury has been occured in various clinical situations such trauma and surgeries.During surgery,excessive reactive oxygen species(ROS)decreases the quality and quantity of osteoblasts and increases the apoptosis of osteoblasts and osteocytes.It has been reported that remifentanil decrease the production of ROS and inflammatory response.In this study,we investigated whether remifentanil has a protective effect against oxidative stress in osteoblasts or not and influence on factors associated with proliferation and differentiation of osteoblasts.Methods: The groups were divided into the following groups; Control : cells were incubated at 37℃ without remifentanil treatment,.H_2O_2 : cells were exposed to 200 μM of H_2O_2 for 2 h.RPC+H_2O_2 : cells were pretreated with 2 ng/ml of remifentanil for 2 h before exposure of H_2O_2.3-MA+RPC+H_2O_2 : cells were pretreated with 1 mM of 3-MA 1h and remifentanil before exposure of H_2O_2.Results: Osteoblast viability and mineralized matrix of bone is increased by remifentanil pretreatment during H_2O_2-induced oxidative stress.Remifentanil pretreatment effectively decreased the rate of apoptotic nuclei in osteoblasts against H_2O_2-induced oxidative stress.In western blot analysis,remifentanil pretreatment increased the expression of bone-related proteins such as Col I,BMP-2,osterix,TGF-β.However,pretreatment with 3-MA inhibited the protective effect of remifentanil against oxidative stress at cell viability,apoptosis,and mineralized matrix formation Conclusions: This study demonstrated that remifentanil reduce oxidative damage in human osteoblasts.And we showed the possibility that autophagy is related with a protective effect of remifentanil in response to oxidative stress.For clinical correlation,further clinical based researches will be needed.