作者: Cristina Angeloni , Cecilia Prata , Francesco Vieceli Dalla Sega , Roberto Piperno , Silvana Hrelia
DOI: 10.1155/2015/370312
关键词: Downregulation and upregulation 、 Surgery 、 Oxidative stress 、 Traumatic brain injury 、 Neuroscience 、 NADPH oxidase 、 Pathophysiology 、 Reactive oxygen species 、 Medicine 、 Poison control 、 Programmed cell death
摘要: Traumatic brain injury (TBI) represents one of the major causes mortality and disability in world. TBI is characterized by primary damage resulting from mechanical forces applied to head as a direct result trauma subsequent secondary due complex cascade biochemical events that eventually lead neuronal cell death. Oxidative stress plays pivotal role genesis delayed harmful effects contributing permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function production reactive oxygen species (ROS), have been shown be source ROS involved several neurological diseases. Emerging evidence demonstrates Nox upregulated after TBI, suggesting critical onset development this pathology. In review, we summarize current about pathophysiology TBI.