【摘要】 目的:通过研究大鼠局灶性脑缺血再灌注(cerebral ischemic reperfusion,CIR)后原肌球蛋白相关激酶(tropom yosin-related kinase,Trk)在不同时间大脑各区的表达特点,采用人尿激肽原酶(human urinary kallikrein,Hk-1)干预后Trk在不同时间大脑缺血区的表达变化及特点,探讨Trk与脑缺血的关系。方法:通过线拴法制作大鼠大脑中动脉缺血(MCAO)再灌注模型,采用免疫组化方法观察急性缺血不同时间脑区及干预后的Trk阳性神经元的动态改变。结果:①在纹状体平面,CIR6h后梗死中心Trk阳性神经元数量急剧下降,在CIR24h组中完全消失。半暗带皮质和海马平面,Trk阳性神经元在CIR6h组中显著增多。②Hk-1干预后从CIR6h始Trk活性均较同期CIR组高。结论:CIR的Trk早期活性增加及24h后持续增加可能是缺血刺激后引起的胶质细胞释放生长因子所致。Hk-1干预后其Trk活性均较模型组高,可能与人尿激肽原酶促进了Trk生存通路有关。更多还原

【Abstract】 Objective To investigate the relationship of tropomyosin-related kinase(Trk) and cerebral ischemia by examining the expression features of Trk following focal cerebral ischemic reperfusion(CIR) and intervention by human urinary kallidinogenase-1(Hk-1) in cerebral regions of rats at different time-point.Methods The experimental animal model of reperfusion was induced by intraluminal suture of middle cerebral artery(MCA),and immunohistochemical method was used to examine the change of positive neurons and expression of Trk in brain tissues after acute ischemia and the intervention at different time point.Results On the section of corpora striata,the number of ERK positive neurons were sharply decreased after 6h of CIR and vanished completely at 24h and the neurons sharply rised after 6h of CIR in the section of penumbra cortex and hippocampus.After the intervention with Hk-1,Trk activivity was increased at 6h as compared with CIR group.Conclusion Increased Trk activity in the rats of CIR may be associated with Trk survival gateway resulted from the intervention of Hk-1.更多还原