Fig. 10

NOX2–ROS is a double-edged sword in focal cerebral ischemic stroke. During the early stage of reperfusion, NADPH oxidase 2 is extensively activated, resulting in excessive ROS production. Excessive ROS cause overgeneration of autophagosomes, which on the one hand induces activation of the NLRP3 inflammasome and mediates the inflammatory response. On the other hand, excessive ROS-dependent autophagy inhibits ischemic stroke-induced vascular growth. These processes aggravate stroke-induced brain damage. However, during the delayed stage of ischemic stroke, low levels of NOX2-induced ROS function as signaling molecules, and they can stimulate low levels of autophagosomes that inhibit NLRP3 inflammasome activation and promote vessel formation, which may be achieved through the activation of the PI3K/Akt/NF-kB signaling pathway, thus alleviating the inflammatory response and facilitating angiogenesis to exert protective effects on the ischemic brain