Ma Di, Feng Liangshu, Deng Fang, Feng Jia-Chun
Department of Neurology and Neuroscience Center, the First Hospital of Jilin University, Changchun 130021, China.
Biomed Res Int. 2017;2017:6891645. doi: 10.1155/2017/6891645. Epub 2017 Apr 4.
Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases. Here we review the novel discovery, mechanism, key factors, and clinical application of ischemic postconditioning and discuss its implications for future research and problem of clinical practice.
减轻缺血再灌注后所观察到的结构和功能缺陷的研究,越来越聚焦于缺血后处理的治疗潜力。近年来,已采用了各种缺血后处理的方法和动物模型。这些众多研究的结果表明,缺血后处理神经保护作用的潜在机制可能涉及自由基生成的减少、钙超载的抑制,以及内源性活性物质的释放、膜通道功能的改变和蛋白激酶的激活。在此,我们综述缺血后处理的新发现、机制、关键因素及临床应用,并讨论其对未来研究的意义及临床实践中的问题。