Ischemic postconditioning as a novel avenue to protect against brain injury after stroke.

Ischemic postconditioning as a novel avenue to protect against brain injury after stroke.
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DOI:
10.1038/jcbfm.2009.13
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发表时间:
2009-05
期刊:
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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其他
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缺血后处理最初是指在再灌注后立即进行的断续再灌注,用于预防心肌和脑梗死中的缺血/再灌注损伤。它已经发展成为一个概念,可以通过广泛的刺激或触发诱导,甚至可以在局灶性缺血后6小时和短暂性全脑缺血后2天进行。在心肌缺血的研究中,后处理的概念被认为是源于缺血预处理或部分/逐渐再灌注,但实际上,后处理的实验早于预处理或部分/逐渐再灌注的实验。本文综述了后处理在各种脑缺血模型中的保护作用及其参数。此后,它提供了深入了解与再灌注损伤和Akt,丝裂原活化蛋白激酶(MAPK),蛋白激酶C(PKC)和ATP敏感性K+(KATP)通道细胞信号通路相关的后处理的保护机制。最后,一些开放的问题和未来的挑战,临床翻译后处理进行了讨论。
Ischemic postconditioning initially referred to a stuttering reperfusion performed immediately after reperfusion, for preventing ischemia/reperfusion injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers, and may even be performed as late as 6 h after focal ischemia and 2 days after transient global ischemia. The concept is thought to be derived from ischemic preconditioning or partial/gradual reperfusion, but in fact the first experiment for postconditioning was carried out much earlier than that of preconditioning or partial/gradual reperfusion, in the research on myocardial ischemia. This review first examines the protective effects and parameters of postconditioning in various cerebral ischemic models. Thereafter, it provides insights into the protective mechanisms of postconditioning associated with reperfusion injury and the Akt, mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and ATP-sensitive K+ (KATP) channel cell signaling pathways. Finally, some open issues and future challenges regarding clinical translation of postconditioning are discussed.
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