Remifentanil Negatively Regulates RANKL-Induced Osteoclast Differentiation and Bone Resorption by Inhibiting c-Fos/NFATc1 Expression.

Remifentanil is commonly used in operating rooms and intensive care units for the purpose of anesthesia and sedation or analgesia. Although remifentanil may significantly affect the bone regeneration process in patients, there have been few studies to date on the effects of remifentanil on bone physiology. The purpose of this study was to investigate the effects of remifentanil on osteoclast differentiation and bone resorption.

Remifentanil induces autophagy and prevents hydrogen peroxide-induced apoptosis in Cos-7 cells.

Background: This study investigated the effect of remifentanil pretreatment on Cos-7 cells exposed to oxidative stress, and the influence of remifentanil on intracellular autophagy and apoptotic cell death.

Methods: Cells were divided into 4 groups: (1) Control: non-pretreated cells were incubated in normoxia (5% CO, 21% O, and 74% N). (2) HO: non-pretreated cells were exposed to HO for 24 h.

Propofol protects against oxidative-stress-induced COS-7 cell apoptosis by inducing autophagy.

Background: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear.