摘要
目的探讨细胞外信号调节激酶(ERK)在局灶性脑缺血/再灌注损伤梗死灶周皮层区的动态时空变化及其作用机制。方法建立兔大脑中动脉阻断(MCAO)局灶性脑缺血再灌注模型,应用免疫组化检测ERK1在脑缺血2h再灌注不同时间灶周皮层的动态表达规律,同时应用免疫组化和流式细胞术检测细胞凋亡状态的动态变化。结果免疫组化分析显示,缺血2h再灌注灶周皮层区1hERK1表达开始增多,6h数目明显增多,3d达高峰,然后逐渐下降,14d回落到基线水平,其阳性细胞数分别为0.22±0.02、0.25±0.02、0.42±0.04、0.14±0.02。其表达时程变化与灶周皮层凋亡的变化相一致。结论脑缺血损伤诱导ERK表达增强,ERK在介导神经细胞凋亡和缺血性损伤中起重要作用。这为脑缺血治疗提供了新的思路。
Objective To investigate the temporospatial alterations and effect of the activation of extracellular signal-regulated kinase I（ERK1） in perifocal cortex involved in cerebral ischemic injury. Methods The cerebral ischemia focally 2 h and reperfusion 72 h model in rabbits was induced by transient occlusion of middle cerebral artery （MCA）. Here the dynamic changes of expression of ERK1 in perifocal cortex of the rabbit brain exposed to 2 h ischemia and different periods of reperfusion were detected by immunohistochemistry. Meantime, the apoptosis status were detected by immunohistochemistry and by flow cytometry methods. Results ERK1 activation was first increased in perifocal cortex at 1 h of reperfusion and strongly activated at 6 h with a peak at 3 d by immuohistochemistry, and gradually decreased to basal level at 14 d of reperfusion（0.22±0. 02,0.25±0. 02,0. 42±0. 04,0. 14±0. 02）. All these were correlated with the change of apoptosis in the perifocal cortex. Conclusions ERK signaling pathway was involved in the ischemic injury and played an important role in apoptosis of neurons and focally cerebral ischemia, this finding may provide a therapeutic apporach for cerebral ischemia.
出处
《中国神经免疫学和神经病学杂志》
CAS
2007年第2期102-104,108,共4页
Chinese Journal of Neuroimmunology and Neurology
关键词
脑缺血再灌注
细胞外信号调节激酶
凋亡
cerebral ischemia reperfusion injury
extracelluar signal-regulated kinase
apoptosis
