CEPO经Mash1信号促进大鼠局部脑缺血后纹状体内神经发生

Carbamylated erythropoietin via Mash1 signaling promotes neurogenesis in the ischemic striatum following focal cerebral ischemia in rats

为检测氨甲酰化促红细胞生成素(CEPO)在大鼠脑缺血后发生过程中的作用及其相关信号通路,本实验将成年大鼠大脑中动脉栓塞(MCAO)后立即尾静脉给予CEPO(50μg/kg)。结果显示:CEPO可显著降低大鼠MCAO后3d梗塞面积,增加缺血侧神经干细胞增殖、促进神经干细胞分化成为神经元。CEPO的促神经发生效应与缺血侧纹状体内前神经元bHLH转录因子Mash1的表达上调密切相关。本结果提示CEPO对脑缺血具有神经保护作用,Mash1信号在缺血侧纹状体内可能介导CEPO增强的神经发生和神经元分化效应。

To investigate the effect of carbamylated erythropoietin （ CEPO ） on neurogenesis and the associated signaling pathways in a model of cerebral ischemia in rats, rats subjected to middle cerebral artery occlusion （MCAO） were treated immediately with CEPO after MCAO. Cerebral infarct volumes were assessed at 3 days post-MCAO. CEPO at a dose of 50μg/kg significantly reduced infarct volume and increased neural stem cells proliferation and promoted neural stem cells differentiation into neurons in the ischemic striatum, which was associated with up-regulation of Mashl, a pro-neuron basic helix-loop-helix protein transcription factor. Taken together, these actions of CEPO are likely to contribute to their neuroprotection following cerebral ischemia; the Mashl signaling pathway may mediate CEPO-en- hanced neurogenesis and neuronal differentiation in the ischemic striatum.