title: [Course of acute oxidative damage after traumatic brain injury: problem and strategy].
abstract: During secondary pathophysiological cascades of early brain injury (EBI) after traumatic brain injury (TBI), reactive oxygen species (ROS) act rapidly play a pivotal role in the pathogenesis, neurodegeneration and prognosis of EBI via damaging lipid, protein and nucleic acid. However, the time spot of biological sample collection of oxidation-stress in TBI animal model lag behind in clinical observation or in theoretical datum. This paradox and the related methodology are reviewed in this paper.
authors.affiliation: 2012 grade, Shanghai Medical College of Fudan University, Shanghai 200403,China.
authors.forename: Yunke
authors.initials: Y
authors.lastname: Huang
authors.forename: Xi
authors.initials: X
authors.lastname: Huang
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species