新生鼠脑缺血预处理后海马CA1区脑源性神经营养因子的表达和意义

目的观察脑缺血预处理对新生Wistar大鼠脑缺血再灌注后海马CAl区脑源性神经营养因子(BDNF)表达的影响和意义。方法通过阻断7日龄新生Wistar大鼠右侧颈总动脉45分钟制备脑缺血模型,设置假手术组、缺血再灌注组和预缺血-缺血再灌注组。采用免疫组化方法和计算机图像分析技术检测3组新生鼠不同时点海马CAl区脑组织BDNF的动态变化及3组光镜下脑组织病理改变。结果(1)脑组织病理改变:预缺血组病理损伤较缺血再灌注组轻。(2)BDNF表达: 预缺血-缺血再灌注组BDNF表达在再灌注后3h开始增高,12h达高峰,24h开始下降,与假手术组和缺血再灌注组比较均有显著性差异(P<0．05),3天降至假手术组水平。结论新生鼠脑缺血预处理早期可诱导海马CAl区BDNF表达和合成增加,对防止再次严重的脑缺血损伤有明显的保护作用, 可能与脑缺血后神经细胞的内源性保护机制有关。

The expression and significance of BDNF in hippocampal CA1 region after cerebral ischemic precon ditioning in neonatal rats

Objective To study the effects and signigficance of cerebral ischemic preconditioning on the expression of brain-derived neurotrophic factor(BDNF) in hippocmpal CA1 region after cerebral ischemia and reperfusion in neonatal Wistar rats. Methods The model of cerebral ischemia in 7-day-old Wistar rat was induced by occluding right arteria carotis communis for 45 minutes. The Wistar rats were randomly divided into three groups: sham-operation group, ischemia-reperfusion group and preischemia-reperfusion group. The pathological changes of the rats' brains were observed by optical microscope, while immunohistochemistry and computer image analysis techniques were used to detect the synthesis of BDNF. Results (1)The pathological manifestation of the brain damage was milder in preischemia-reperfusion group than in ischemia-reperfusion group. (2) The synthesis of BDNF in hipp-ocampal CA1 region in preischemia-reperfusion group increased 3h after reperfusion, reached the peak after 12h, then began to decline after 24h, and gradually declined to the sham group level after 3d. The synthesis of BDNF in preischemia-reperfusion group had the significant difference when compared with other two groups (P<0. 05). Conclusion The cerebral ischemic preconditioning in neonatal rats can increase the expression and sythesis of BDNF in hippocampal CA1 region, which can provide neu-roprotective effect for a subsequent severe cerebral ischemic insult. And this protection may concern on the endogenous protective mechanism of neuron after the cerebral ischemia.