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目的探讨永久性前脑缺血大鼠海马CA1区脑源性神经营养因子(BDNF)及其受体酪氨酸蛋白激酶B(TrkB)蛋白表达水平的改变。方法采用永久性结扎双侧颈总动脉的方法制造永久性前脑缺血大鼠模型。造模8周后对大鼠大脑石蜡切片进行免疫组织化学染色,测定海马CA1区BDNF以及TrkB的定位、相对定量表达。抽提大鼠海马CA1区组织蛋白,采用Western Blot对BDNF以及TrkB的蛋白表达水平进行定量分析。结果永久性前脑缺血8周后,大鼠海马CA1区BDNF免疫反应阳性产物主要分布于锥体细胞的胞浆、胞核及轴突;模型组大鼠的BDNF蛋白表达水平显著升高(P<0.05)。大鼠海马CA1区TrkB免疫反应阳性产物主要分布于神经元的胞浆及轴突内;与假手术组相比,模型组大鼠海马CA1区TrkB蛋白表达水平无显著改变(P>0.05)。结论双侧颈总动脉结扎造成的永久性前脑缺血可增加大鼠海马CA1区BDNF蛋白表达水平,而对其受体TrkB的蛋白表达水平无显著影响。
Objective To investigate the expression of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) protein in hippocampal CA1 area of permanent forebrain ischemia rats. Methods A permanent forebrain ischemia rat model was established by permanent ligation of bilateral common carotid arteries. After 8 weeks of modeling, paraffin sections of rat brain were immunohistochemically stained to determine the localization and relative quantitative expression of BDNF and TrkB in hippocampal CA1 area. The hippocampal CA1 region of rat hippocampus tissue protein was extracted, Western Blot quantitative analysis of BDNF and TrkB protein levels. Results After 8 weeks of permanent forebrain ischemia, BDNF immunoreactive products in the hippocampal CA1 region were mainly distributed in the cytoplasm, nucleus and axon of the pyramidal cells. The BDNF protein expression in the model group was significantly increased P <0.05). The TrkB immunoreactive products in the hippocampal CA1 region were mainly distributed in the cytoplasm and axon of neurons. Compared with the sham operation group, the TrkB protein expression in the hippocampal CA1 region of the model group had no significant change (P> 0.05). Conclusion Permanent forebrain ischemia caused by bilateral common carotid artery ligation can increase BDNF protein expression in rat hippocampal CA1 region, but has no significant effect on its receptor TrkB protein expression.