The underlying mechanisms involved in the protective effects of ischemic postconditioning

Cerebral ischemic postconditioning (PostC) refers to a series of brief ischemia and reperfusion (I/R) cycles applied at the onset of reperfusion following an ischemic event. PostC has been shown to have neuroprotective effects, and represents a promising clinical strategy against cerebral ischemia-reperfusion injury. Many studies have indicated that cerebral PostC can effectively reduce neural cell death, cerebral edema and infarct size, improve cerebral circulation, and relieve inflammation, apoptosis and oxidative stress. In addition, several protective molecular pathways such as Akt, mTOR and MAPK have been shown to play a role in PostC-induced neuroprotection. PostC represents an attractive therapeutic option because of its ability to be induced rapidly or in a delayed fashion, as well as being inducible by pharmacological agents. As a potential clinical treatment, PostC is therapeutically translatable as it can be induced remotely. The underlying mechanisms of PostC have been systematically investigated, but still need to be comprehensively analyzed. As most PostC studies to date were conducted preclinically using animal models, future studies are needed to optimize protocols in order to accelerate the clinical translation of PostC.