Qin Wenjing, Li Zhendong, Luo Shijian, Wu Rui, Pei Zhong, Huang Ruxun
Department of Neurology, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai 519000, China.
Department of Neurology, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai 519000, China.
Neurosci Lett. 2014 May 21;569:80-4. doi: 10.1016/j.neulet.2014.03.052. Epub 2014 Apr 1.
Fractalkine/CX3CL1, also called neurotactin, has been described as an angiogenic agent, and its expression is up-regulated in the penumbra after ischemia. This study was conducted to investigate the neovascular potential of fractalkine on rat models of transient middle cerebral artery occlusion (MCAO). Rats receiving intracerebroventricular injections of fractalkine were found to have improved neurological deficits, reduced cerebral infarct size and increased neuron survival for both doses (100ng and 1μg). Fractalkine exerted angiogenic effects that showed dose-dependent higher vascular densities in the peri-infarct area. Furthermore, exogenous fractalkine increased the proliferation of endothelial cells in a dose-dependent manner and enhanced the migration of endothelial progenitor cells at the higher dose (1μg) in ischemic penumbra. In conclusion, intracerebroventricular administration of fractalkine reduces ischemic damage by promoting neuroprotection and by inducing endothelial cell proliferation and endothelial progenitor cell migration, thereby enhancing neovascularization in the peri-infarct region.
趋化因子/CX3CL1，也称为神经趋化蛋白，已被描述为一种血管生成因子，其表达在缺血后的半暗带中上调。本研究旨在探讨趋化因子在短暂性大脑中动脉闭塞（MCAO）大鼠模型中的新生血管形成潜力。发现接受脑室内注射趋化因子的大鼠，两种剂量（100ng和1μg）均有神经功能缺损改善、脑梗死面积减小和神经元存活率增加的情况。趋化因子发挥了血管生成作用，在梗死周边区域显示出剂量依赖性的更高血管密度。此外，外源性趋化因子以剂量依赖性方式增加内皮细胞的增殖，并在较高剂量（1μg）时增强缺血半暗带中内皮祖细胞的迁移。总之，脑室内给予趋化因子可通过促进神经保护以及诱导内皮细胞增殖和内皮祖细胞迁移来减少缺血损伤，从而增强梗死周边区域的新生血管形成。
