论文部分内容阅读
为了研究成年大鼠局灶性脑缺血后侧脑室室下区(SVZ)神经发生的情况及其与血管内皮生长因子(VEGF)的关系,探讨脑缺血后神经发生及其调控机制,本研究通过大脑中动脉阻断法(MCAO)建立大鼠局灶性脑缺血模型,5-溴-2-脱氧尿核苷(BrdU)标记增殖的神经前体细胞,用免疫荧光双标记法动态检测BrdU、TuJ1、MAP-2、GFAP的表达,同时观察增殖细胞表达VEGF及其受体情况。结果显示:与对照组相比,大鼠SVZ的BrdU阳性细胞数在脑缺血后4 d组明显增加,14 d组达到高峰;Br-dU/TuJ1、BrdU/MAP-2阳性双标细胞数在脑缺血后14 d组开始增加,28 d组达到高峰;但BrdU/GFAP阳性双标细胞数则无明显变化;增殖的BrdU阳性细胞同时表达VEGF及其受体FLK-1。以上结果提示:大鼠局灶性脑缺血可激活SVZ自体神经前体细胞原位增殖、分化,且增殖的细胞同时表达VEGF及其受体可能是脑缺血后神经发生增强的调节机制之一。
To investigate the neurogenesis in the subventricular zone (SVZ) of adult rats after focal cerebral ischemia and its relationship with vascular endothelial growth factor (VEGF), to explore the mechanism of neurogenesis and its regulation after cerebral ischemia A rat model of focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO). Proliferation of neural precursor cells labeled with 5-bromo-2-deoxyuridine (BrdU) was studied by immunofluorescence double labeling The expression of BrdU, TuJ1, MAP-2 and GFAP were detected, and the expression of VEGF and its receptor in proliferating cells were also observed. The results showed that compared with the control group, the number of BrdU-positive cells in SVZ increased significantly at 4 d after cerebral ischemia and peaked at 14 d. The number of BrdU / TuJ1 and BrdU / MAP-2 positive double-labeled cells The number of BrdU / GFAP positive double-labeled cells did not change significantly at 14d after cerebral ischemia, and peaked at 28d. The proliferation of BrdU-positive cells also expressed VEGF and its receptor FLK-1. These results suggest that: focal cerebral ischemia in rats can activate SVZ autologous neural progenitor cells in situ proliferation and differentiation, and proliferation of cells expressing VEGF and its receptor may be neurogenesis after cerebral ischemia regulatory mechanism one.