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It is difficult to control the degree of ischemic postconditioning in the brain and other isch-emia-sensitive organs. Remote ischemic postconditioning could protect some ischemia-sensitive organs through measures on terminal organs. In this study, a focal cerebral ischemia-reperfusion injury model was established using three cycles of remote ischemic postconditioning, each cycle consisted of 10-minute occlusion of the femoral artery and 10-minute opening. The results showed that, remote ischemic postconditioning signiifcantly decreased the percentage of the in-farct area and attenuated brain edema. In addition, inlfammatory nuclear factor-κB expression was signiifcantly lower, while anti-apoptotic Bcl-2 expression was signiifcantly elevated in the ce-rebral cortex on the ischemic side. Our ifndings indicate that remote ischemic postconditioning attenuates focal cerebral ischemia/reperfusion injury, and that the neuroprotective mechanism is mediated by an anti-apoptotic effect and reduction of the inlfammatory response.
