原肌球蛋白受体激酶在脑缺血大鼠各脑区的表达特性

Expression Pattern of Tropomyosin Receptor Kinase after Focal Cerebral Ischemia in Rat

目的观察大鼠局灶性脑缺血后神经营养因子受体原肌球蛋白受体激酶(Trk)在大脑各区的表达特点,探讨其与缺血损伤的关系。方法制作大鼠局灶性脑缺血模型,采用免疫组化方法观察急性缺血不同时间脑区Trk阳性神经元的动态改变。结果正常脑组织中Trk受体广泛表达,缺血后梗死中心Trk表达急剧下降,1 d后完全消失;而半暗带及海马DG区Trk阳性神经元自缺血6 h开始显著增多(P<0.05),持续整个缺血期。海马CA1区于缺血1 d后Trk表达开始缓慢升高;缺血侧的其他脑区及对侧非缺血脑区也有Trk表达升高。结论缺血损伤可诱导脑内Trk受体表达广泛增加,与内源性神经保护机制有关。

Objective To investigate the expression pattern of tropomyosin receptor kinase （Trk） after focal cerebral ischemia in rat, and to explore the relationship between ischemia and the pattern of Trk expression. Methods The model of focal cerebral ischemia was built by middle cerebral artery occlusion. Immunocytochemistry staining was used to observe the dynamic changes of Trk expression at different time of acute stage of ischemia, and the patterns at different regions of the striate and hippocampal were detected. Results Trk immuno-positive neurons widely expressed in the normal brain. The number of Trk immuno-positive neurons was decreased abruptly in the necrosis core of the focal cerebral of ischemia, while increased obviously in the penumbra region and the DG area after 6 h of occlusion（P 〈0.05）, and existed consecutively. The increasing expression trend was also detected in other regions of the brain, including the contralateral non-ischemia part. In contrast, the number of positive neurons increased slowly in the＂ CA1 region after ischemia. Conclusion Ischemia injury can induce the wide expression of Trk in brain. It may be related to the endogenetic neuro-protective reaction.