摘要
目的:探讨局灶性脑缺血再灌注损伤后谷氨酸受体NMDAR1蛋白表达的变化及意义。方法:2002-08/2003-03在山东大学医学院病理生理研究所进行。观察大鼠大脑中动脉闭塞2h再灌0,1,3,6,9,12,24,72h,1周、2周10个时相点脑的病理及NMDAR1免疫组化染色变化。结果:苏木精-伊红染色显示大脑中动脉闭塞后脑组织出现神经细胞变性,细胞周围水肿,软化灶等改变。免疫组化染色显示正常大鼠大脑皮质及皮质下神经细胞NMDAR1呈散在阳性表达,胶质细胞无表达。缺血再灌0～1hNMDAR1表达即明显增高,3h左右达高峰,然后逐渐下降,24～72h表达明显低于正常,一两周表达开始恢复。结论:脑缺血后NMDAR表达的变化参与了脑缺血的病理生理过程,早期表达的升高是谷氨酸兴奋性细胞毒性作用的重要环节,后期表达的下降可能不利于神经功能的恢复。
AIM:To study the changes and significance of the protein expression of N methyl D asparate receptor 1(NMDAR1) in rats after local ischemia reperfusion injury. METHODS:The experiment was finished in the Institute of Phathophysiology,Medical College of Shandong University from August 2002 to March 2003.The To observe the pathological changes and NMDAR1 immunohistochemical staining in rats with reperfusion at intervals of 0,1,3,6,9,12,24 and 72 hours,1 and 2 weeks after middle cerebral artery occlusion(MCAO). RESULTS:HE staining showed that neuron degeneration,tissue edema and focal softening were observed in the brain after MCAO.Immunohistochemical staining showed that there were moderate NMDAR1 positive expression in neuron but no expression in glial cells in cerebral cortex and subcortex of normal rats.The NMDAR1 expression increased sharply after 0 to 1 hour reperfusion,and reached the peak value at 3 hour after reperfusion,then decreased gradually and had a lower expression during 24 to 72 hours after reperfusion,and the expression began to rise at 1 to 2 weeks after reperfusion. CONCLUSION:The changes of NMDAR protein expression in cerebral ischemia takes part in the pathophysilogical process of cerebral ischemia.The increased expression in earlier period is an important link of the excitotoxic mechanisms of glutamate and the lower expression in the later period is not good for the recover of the neurological function.
出处
《中国临床康复》
CSCD
2004年第34期7688-7689,共2页
Chinese Journal of Clinical Rehabilitation
