Protective effects of remifentanil against H2O2-induced oxidative stress in human osteoblasts
윤지영, 김도완, 김은정, 박봉수, 윤지욱, 김형준, 박정훈,
소속 상세정보
윤지영 ( Yoon Ji-Young ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
김도완 ( Kim Do-Wan ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
김은정 ( Kim Eun-Jung ) - 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
김형준 ( Kim Hyung-Joon ) - Pusan National University School of Dentistry Department of Oral Physiology
박정훈 ( Park Jeong-Hoon ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
KMID : 0980320160160040263
Abstract
Background: Bone injury is common in many clinical situations, such as surgery or trauma. During surgery, excessive reactive oxygen species (ROS) production decreases the quality and quantity of osteoblasts. Remifentanil decreases ROS production, reducing oxidative stress and the inflammatory response. We investigated remifentanil's protective effects against H2O2-induced oxidative stress in osteoblasts.
Methods: To investigate the effect of remifentanil on human fetal osteoblast (hFOB) cells, the cells were incubated with 1 ng/ml of remifentanil for 2 h before exposure to H2O2. For induction of oxidative stress, hFOB cells were then treated with 200 μM H2O2 for 2 h. To evaluate the effect on autophagy, a separate group of cells were incubated with 1 mM 3-methyladenine (3-MA) before treatment with remifentanil and H2O2. Cell viability and apoptotic cell death were determined via MTT assay and Hoechst staining, respectively. Mineralized matrix formation was visualized using alizarin red S staining. Western blot analysis was used to determine the expression levels of bone-related genes.
Results: Cell viability and mineralized matrix formation increased on remifentanil pretreatment before exposure to H2O2-induced oxidative stress. As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and TGF-β). However , pretreatment with 3-MA before exposure to remifentanil and H2O2 inhibited remifentanil's protective effects on hFOB cells during oxidative stress.
Conclusions: We showed that remifentanil prevents oxidative damage in hFOB cells via a mechanism that may be highly related to autophagy. Further clinical studies are required to investigate its potential as a therapeutic agent.
키워드
Autophagy; Osteoblasts; Oxidative Stress; Remifentanil
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