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原位和远程缺血后处理的干预方法和脑保护机制的研究进展。

Advances in intervention methods and brain protection mechanisms of in situ and remote ischemic postconditioning.

机构信息

Institute of Neuroscience, Kunming Medical University, Kunming, 650500, Yunnan, China.

Second Department of General Surgery, First People's Hospital of Yunnan Province, Kunming, 650032, Yunnan, China.

出版信息

Metab Brain Dis. 2021 Jan;36(1):53-65. doi: 10.1007/s11011-020-00562-x. Epub 2020 Oct 12.

DOI:10.1007/s11011-020-00562-x
PMID:33044640
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.

摘要

缺血后处理(PostC)通常是指一系列短暂的血管闭塞和再灌注,它可以诱导内源性神经保护作用,减轻脑缺血/再灌注(I/R)损伤。根据适应性缺血干预的部位,PostC 可分为局部缺血后处理(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、减少抗氧化应激和抗神经元凋亡、减轻脑水肿以及调节自噬以及 Akt、MAPK、PKC 和 KATP 通道细胞信号通路等保护机制来减轻脑 I 损伤。然而,很少有研究比较 ISPostC 和 RIPostC 干预的干预方法、保护机制和细胞信号通路。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。

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本文引用的文献

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Peptide Sodium Channels Modulator Mu-Agatoxin-Aa1a Prevents Ischemia-Reperfusion Injury of Cells.肽钠通道调节剂 Mu-Agatoxin-Aa1a 可预防细胞缺血再灌注损伤。
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