摘要
目的 研究短暂性脑缺血再灌注损伤时微管相关蛋白 (MAP2 )表达的动态变化及意义。方法 采用沙土鼠一过性前脑缺血再灌注模型 ,以免疫组织化学染色法 ,观察缺血 5 m in再灌注 0 h、3h、2 4h、48h、72 h、7d海马区 MAP2 表达的动态变化以及观察相应时间点海马区神经元病理组织学变化。结果 在正常的沙土鼠脑内 ,神经元呈 MAP2 染色阳性反应 ,在缺血 5 min再灌注后 ,海马区出现了 MAP2 染色减弱或消失区 ,随再灌注时间的延长 ,染色减弱或消失区扩大 ,但主要限于海马区 ,相应神经元的病理组织学变化也随再灌注时间的延长而加重。结论 MAP2 免疫组织化学法可显示神经元形态及脑缺血超早期病变 ;短暂性脑缺血再灌注损伤在脑内并不是均一地发生 ,而是存在着选择性易损伤区 ,海马 CA1 区发生了广泛的迟发性神经元死亡 ;MAP2 的分解破坏或合成障碍 ,可能参与了脑缺血再灌注的损伤机制。
Objective To study the effects of MAP 2 expression on delayed neuronal death in gerbil. Methods The expression,distribution and developmental changes of MAP 2 were examined by means of immunohistochemical assay in the gerbils forebrain ischemia models performed by occluding CCA for 5 minutes. Results The MAP 2 was expressed constitutively in the neuron of cortex and hippocampus of normal gerbil. After ischemia for 5 minutes,a small number of pyramidal cells in the CA 1 area of the hippocampus lost their reaction to the antiserum. The MAP 2 immunoactivity from 48h after reperfusion diminished rapidly in the hippocampal CA 1. Conclusion The delayed neuronal death is not equably distributed in the hippocampus but has selected vulnerable regions. Decomposition of MAP 2 may participate the process of delayed neuronal death.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2002年第3期139-141,共3页
Journal of Apoplexy and Nervous Diseases