| Literature DB >> 33044640 |
Jian-Hui Guo1, Li-Yan Li2, Chun-Yan Li3, Wei Ma3, Kuang-Pin Liu3, Jin-Wei Yang4, Xian-Bin Wang3, Zhen Wu4, Tong Zhang4, Jia-Wei Wang4, Wei Liu3, Jie Liu3, Yu Liang3, Xing-Kui Zhang3, Jun-Jun Li3.
Abstract
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.Entities:
Keywords: In situ ischemic postconditioning; Ischemic postconditioning; Ischemic stroke; Neuroprotection; Remote ischemic postconditioning
Year: 2020 PMID: 33044640 DOI: 10.1007/s11011-020-00562-x
Source DB: PubMed Journal: Metab Brain Dis ISSN: 0885-7490 Impact factor: 3.584