Pignataro Giuseppe, Scorziello Antonella, Di Renzo Gianfranco, Annunziato Lucio
Division of Pharmacology, Department of Neuroscience, School of Medicine, Federico II University of Naples, Italy.
FEBS J. 2009 Jan;276(1):46-57. doi: 10.1111/j.1742-4658.2008.06769.x.
Because clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Two endogenous mechanisms have been characterized so far, namely ischemic preconditioning and ischemic postconditioning. The neuroprotective concept of preconditioning is based on the observation that a brief, noninjurious episode of ischemia is able to protect the brain from a subsequent longer ischemic insult. Recently, a hypothesis has been offered that modified reperfusion subsequent to a prolonged ischemic episode may also confer ischemic neuroprotection, a phenomenon termed postconditioning. Many pathways have been proposed as plausible mechanisms to explain the neuroprotection offered by preconditioning and postconditioning. Unfortunately, so far, none of them has clearly identified the mechanism involved in preconditioning and postconditioning. The present article will review the main mechanisms reported to date to explain the neuroprotective effect of both ischemic preconditioning and postconditioning.
由于中风药理学神经保护策略的临床试验令人失望，人们的注意力已转向大脑自身的内源性神经保护策略。迄今为止，已明确了两种内源性机制，即缺血预处理和缺血后处理。预处理的神经保护概念基于这样的观察结果：短暂的、非损伤性的缺血发作能够保护大脑免受随后更长时间的缺血损伤。最近，有人提出一种假说，即长时间缺血发作后的改良再灌注也可能赋予缺血性神经保护作用，这一现象被称为后处理。许多途径已被提出作为解释预处理和后处理所提供神经保护作用的合理机制。不幸的是，到目前为止，它们中没有一个能明确识别出参与预处理和后处理的机制。本文将综述迄今为止报道的解释缺血预处理和缺血后处理神经保护作用的主要机制。
