Ischemic postconditioning (PostC) conventionally refers to a series of brief blood vessel occlusions and reperfusions, which can induce an endogenous neuroprotective effect and reduce cerebral ischemia/reperfusion (I/R) injury. Depending on the site of adaptive ischemic intervention, PostC can be classified as in situ ischemic postconditioning (ISPostC) and remote ischemic postconditioning (RIPostC). Many studies have shown that ISPostC and RIPostC can reduce cerebral IS injury through protective mechanisms that increase cerebral blood flow after reperfusion, decrease antioxidant stress and anti-neuronal apoptosis, reduce brain edema, and regulate autophagy as well as Akt, MAPK, PKC, and KATP channel cell signaling pathways. However, few studies have compared the intervention methods, protective mechanisms, and cell signaling pathways of ISPostC and RIPostC interventions. Thus, in this article, we compare the history, common intervention methods, neuroprotective mechanisms, and cell signaling pathways of ISPostC and RIPostC.

缺血后处理（PostC）通常是指一系列短暂的血管闭塞和再灌注，可以诱导内源性神经保护作用并减少脑缺血/再灌注（I/R）损伤。根据适应性缺血干预的部位，PostC 可分为原位缺血后处理 (ISPostC) 和远程缺血后处理 (RIPostC)。许多研究表明，ISPostC和RIPostC可以通过增加再灌注后脑血流量、降低抗氧化应激和抗神经元凋亡、减轻脑水肿、调节自噬以及Akt、MAPK、PKC和KATP 通道细胞信号通路。然而，很少有研究比较干预方法、保护机制、ISPostC 和 RIPostC 干预的细胞信号通路。因此，在本文中，我们比较了 ISPostC 和 RIPostC 的历史、常见干预方法、神经保护机制和细胞信号通路。