Minnerup Jens, Sevimli Sevgi, Schäbitz Wolf-Rüdiger
Department of Neurology, University of Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany.
Exp Transl Stroke Med. 2009 Oct 21;1:2. doi: 10.1186/2040-7378-1-2.
G-CSF is widely employed for the treatment of chemotherapy-induced neutropenia. Recently, neuroprotective effects of G-CSF in animal stroke models were discovered including infarct size reduction and enhancement of functional recovery. The underlying mechanisms of action of G-CSF in ischemia appear to be a direct anti-apoptotic activity in neurons and a neurogenesis inducing capacity. Additional effects may be based on the stimulation of new blood-vessel formation, the stimulation of immunocompetence and -modulation as well as on bone marrow mobilization. In addition to a discussion of these mechanisms, we will review the available preclinical studies and analyze their impact on the overall efficacy of G-CSF in experimental stroke.
粒细胞集落刺激因子(G-CSF)被广泛用于治疗化疗引起的中性粒细胞减少症。最近,在动物中风模型中发现了G-CSF的神经保护作用,包括梗死面积减小和功能恢复增强。G-CSF在缺血中的潜在作用机制似乎是对神经元的直接抗凋亡活性和诱导神经发生的能力。其他作用可能基于刺激新血管形成、刺激免疫能力和调节以及骨髓动员。除了讨论这些机制外,我们还将回顾现有的临床前研究,并分析它们对G-CSF在实验性中风中的总体疗效的影响。