Li Wenjun, Yang Shaohua
Center for Neuroscience Discovery, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Brain Circ. 2016 Oct-Dec;2(4):153-163. doi: 10.4103/2394-8108.195279. Epub 2016 Dec 6.
Excessive oxygen and its chemical derivatives, namely reactive oxygen species (ROS), produce oxidative stress that has been known to lead to cell injury in ischemic stroke. ROS can damage macromolecules such as proteins and lipids and leads to cell autophagy, apoptosis, and necrosis to the cells. This review describes studies on the generation of ROS, its role in the pathogenesis of ischemic stroke, and recent development in therapeutic strategies in reducing oxidative stress after ischemic stroke.
过量的氧气及其化学衍生物,即活性氧(ROS),会产生氧化应激,已知其会导致缺血性中风中的细胞损伤。ROS会损害蛋白质和脂质等大分子,并导致细胞自噬、凋亡和坏死。本文综述了关于ROS的产生、其在缺血性中风发病机制中的作用以及缺血性中风后降低氧化应激的治疗策略的最新进展。