Oxidase and its inhibitors after getting the ticket and cerebral ischemia-reperfusion injury

Abstract

In ischemic cerebrovascular disease, the release of reactive oxygen species (ROS) is too much, and after reperfusion, it exceeds the body's antioxidant capacity, which eventually leads to brain tissue damage. Therefore, antioxidant therapy is considered as a treatment for ischemic cerebrovascular disease, but clinical trials have not yet been able to translate this concept into a treatment plan for patients. As a transformation of this concept, the most important research at present is the source of ROS, not ROS itself. In this context, NADPH oxidase (NOX) has been identified as the main producer of ROS in the cerebrovascular system under normal physiological conditions and ischemia-reperfusion, which is mainly involved in oxidative stress, mediating autophagy, inflammation, etc. . Inhibition of NOX can significantly reduce ischemic injury in stroke, but the distribution and activation mechanism of each subtype of NOX family are different, so it is necessary to clarify its mechanism and the significance of using inhibitor therapy. This paper reviews the structure of NOX, its mechanism of action in cerebral ischemia-reperfusion injury and the research progress of its inhibitors. [International Journal of Neurology and Neurosurgery, 2021, 48(6):554-558.]