摘要
目的:探讨N-甲基-D-天冬氨酸(NMDA)受体亚单位NR2B特异性拮抗剂Ro25-6981对缺血再灌注大鼠脑室下区神经干细胞增殖的影响及可能的机制。方法:线栓法制作大鼠大脑中动脉栓塞2 h再灌注模型,随机分成假手术组、缺血再灌注对照组和Ro25-6981干预组。免疫组织化学显色观察脑室下区巢蛋白和增殖细胞核抗原(PCNA)阳性细胞数,行免疫印迹对缺血侧脑组织脑源性神经营养因子(BDNF)蛋白表达水平进行定量分析。结果:缺血再灌注后脑室下区巢蛋白和PCNA阳性细胞较假手术组增加,而Ro25-6981干预组巢蛋白和PCNA阳性细胞较缺血再灌注对照组减少。缺血再灌注损伤促进了缺血侧脑组织BDNF蛋白的表达,Ro25-6981干预下调了缺血侧脑组织BDNF蛋白的表达。结论:NMDA受体亚单位NR2B能促进脑室下区神经干细胞的增殖,可能与调节BDNF表达有关。
Objective： To investigate the role of Ro25-6981, NR2B specific antagonist, on proliferation of neural stem cells in ischemia-reperfusion rats. Methods： The model of transient brain ischemia followed by 2 hours reperfusion was induced by practicing middle cerebral artery occlusion. Male SD rats were randomly divided into sham group, ischemia-reperfusion control group and Ro25-6981 treatment group. Number of nestin and proliferating cell nuclear antigen （PCNA） positive cells stained by immunohistochemical method in the subventricular zone （SVZ）. The expression of brain-derived neurotrophic factor （BDNF） was measured by Western blotting. Results： Compared to the sham group, the ischemia：reperfusion group showed the obviously increased number of nestin and PCNA positive cells in the SVZ. However, Number of nestin and PCNA positive cells in Ro25-6981 treatment group decreased compared with control group. Ischemia-reperfusion injury significantly enhanced BDNF protein expression. In contrast, NR2B specific antagonist Ro25-6081 significantly decreased BDNF protein expression. Conclusion： NR2B, the subunit of NMDA receptors, promotes proliferation of neural stem cells in the SVZ, which may be related to the regulation of BDNF expression.
出处
《解剖学杂志》
CSCD
北大核心
2017年第4期425-428,共4页
Chinese Journal of Anatomy
基金
江苏省卫生厅资助项目(H201319)
