Fig. 2

The mechanism of ischemic injury in acute stroke. In the context of acute ischemic stroke (AIS), the obstruction of cerebral blood flow results in damage to cerebral vascular endothelial cells and increased permeability of the blood–brain barrier (BBB). This compromise of the BBB leads to vasogenic cerebral edema, elevated intracranial pressure, and an imbalance in the neuronal microenvironment. Within the framework of AIS, injured neurons may release damage-associated molecular patterns (DAMPs), which subsequently stimulate the production of pro-inflammatory cytokines, including IL-8 and tumor necrosis factor-alpha (TNF-α). The release of cytokines exacerbates cerebral injury by promoting inflammatory responses and neuronal apoptosis. I/R therapy remains a crucial strategy in the management of AIS, as it alleviates both ischemic and reperfusion injuries, thereby protecting cerebral tissue and facilitating neurological recovery. (Created using Adobe Illustrator)