Background: Propofol (2, 6-diisopropylphenol), an intravenous anesthetic has been widely used for inducing and maintaining anesthesia.Apart from its multiple anesthetic advantages, propofol has been reported to have a number of nonanesthetic effects such as anti-oxidative and anti-inflammatory properties.Increasing researches have demonstrated that propofol possesses remarkable protective effects against neuronal injury by inhibiting oxidative stress in vivo and in vitro.However, the underlying mechanisms remain unclear.Oxidative stress plays an important role in the pathology of many central nervous system (CNS) disorders, including Alzheimers disease, Parkinsons disease, and ischemic stroke.The NADPH oxidase (NOX) is a multisubunit complex composed of two membrane-bound subunits (p22phox and gp91phox) and four cytoplasmic subunits (p40phox, p47phox, p67phox and Rac), of which p91phox subunit (NOX2) is the catalytic core that responsible for the electrons transmission to generate ROS, activation of neuronal NADPH oxidase contributes to oxidative injury in the brain, and inhibition of NADPH oxidase can attenuate cerebral oxidative stress.Hydrogen peroxide (-2O2) is produced at nearly every stage of the oxidative cycle and widely applied to induce oxidative stress in vitro.This study aims to investigate the effects of propofol on H2O2-induced oxidative stress in neural cells and examined whether the protective effects involving the modulation ofNADPH oxidase.