van der Kooij Michael A, Groenendaal Floris, Kavelaars Annemieke, Heijnen Cobi J, van Bel Frank
Laboratory for Psychoneuroimmunology, University Medical Center Utrecht, Utrecht, The Netherlands.
Brain Res Rev. 2008 Nov;59(1):22-33. doi: 10.1016/j.brainresrev.2008.04.007. Epub 2008 May 1.
Besides its established function in erythropoiesis, erythropoietin (EPO) is currently also appreciated for its neuroprotective effects. The detrimental sequelae of prolonged cerebral hypoxia and ischemia have been shown to attenuate by EPO treatment. After binding to the EPO receptor, EPO is capable of initiating a cascade of events which--via different pathways--may lead to neuroprotection. The circumstances that determine which specific signalling route(s) are activated by EPO are largely unknown. We aim to provide the reader with a timely overview on the use of EPO in models of stroke and hypoxia-ischemia and to discuss the molecular events that underlie its neuroprotection.
除了其在红细胞生成中已确定的功能外，促红细胞生成素（EPO）目前还因其神经保护作用而受到重视。长期脑缺氧和缺血的有害后遗症已被证明可通过EPO治疗得到减轻。与EPO受体结合后，EPO能够启动一系列事件，这些事件通过不同途径可能导致神经保护。决定EPO激活哪些特定信号通路的情况在很大程度上尚不清楚。我们旨在为读者及时概述EPO在中风和缺氧缺血模型中的应用，并讨论其神经保护作用背后的分子事件。
