Excessive reactive oxygen species （ROS） is released in ischemic cerebrovascular disease， which exceeds the body’s antioxidant capacity after reperfusion and finally leads to brain tissue damage. Therefore， antioxidant treatment has been considered a therapeutic method for ischemic cerebrovascular disease， but clinical trials have not yet been able to promote the translation of this concept into patient treatment regimens. As the translation of this concept， current studies mainly focus on the source of ROS， rather than ROS itself. In this context， NADPH oxidases （NOX） have been identified as important generators of ROS in the cerebrovascular system under general physiological conditions and during ischemia/reperfusion， and they mainly participate in oxidative stress and mediate autophagy and inflammation. Inhibition of NOX can significantly reduce ischemic injury in stroke， but the subtypes of the NOX family vary in distribution and activation mechanism， so it is necessary to clarify its mechanism and the significance of using inhibitors for treatment. This article reviews the research advances in the structure of NOX， its mechanism of action in cerebral ischemia/reperfusion injury， and related inhibitors.