Ischemia-reperfusion injury is a common feature of ischemic stroke, which occurs when blood supply is restored after a period of ischemia. Reperfusion can be achieved either by thrombolysis using thrombolytic reagents such as tissue plasminogen activator (tPA), or through mechanical removal of thrombi. Spontaneous reperfusion also occurs after ischemic stroke. However, despite the beneficial effect of restored oxygen supply by reperfusion, it also causes deleterious effect compared with permanent ischemia. With the recent advancement in endovascular therapy including thrombectomy and thrombus disruption, reperfusion-injury has become an increasingly critical challenge in stroke treatment. It is therefore of extreme importance to understand the mechanisms of ischemia-reperfusion injury in the brain in order to develop effective therapeutics. Accumulating experimental evidence have suggested that the mechanisms of ischemia-reperfusion injury include oxidative stress, leukocyte infiltration, platelet adhesion and aggregation, complement activation, mitochondrial mediated mechanisms, and blood-brain-barrier (BBB) disruption, which altogether ultimately lead to edema or hemorrhagic transformation (HT) in the brain. Potential therapeutic strategies against ischemia-reperfusion injury may be developed targeting these mechanisms. In this review, we briefly discuss the pathophysiology and cellular and molecular mechanisms of cerebral ischemia-reperfusion injury, and potential therapeutic strategies.
Keywords: Blood-brain-barrier; Complement; Ischemia; Leukocyte; Mitochondria; Oxidative stress; Platelet aggregation; Post-conditioning; Reperfusion; Stroke.