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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 detect the role of carbamated erythropoietin (CEPO) in the pathogenesis of cerebral ischemia in rats and its related signaling pathways, CEPO was given to tail vein immediately after middle cerebral artery occlusion (MCAO) in adult rats (50 μg / kg). The results showed that: CEPO can significantly reduce the infarct area of rats after 3 days, increase the proliferation of ischemic neural stem cells and promote the differentiation of neural stem cells into neurons. The neurogenic effect of CEPO is closely related to the up-regulation of Mash1, an inhibitor of bHLH transcription in prefrontal neurons of ischemic striatum. The results suggest that CEPO has a neuroprotective effect on cerebral ischemia. Mash1 signaling may mediate enhanced neurogenesis and neuronal differentiation induced by CEPO in ischemic striatum.