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N-甲基-D-天门冬氨酸受体亚型NR1、NR2A在大鼠视网膜缺血再灌注损伤模型中的表达
引用本文:杜改萍,张世杰,王竫华. N-甲基-D-天门冬氨酸受体亚型NR1、NR2A在大鼠视网膜缺血再灌注损伤模型中的表达[J]. 眼科, 2003, 12(3): 170-174
作者姓名:杜改萍  张世杰  王竫华
作者单位:1. 青岛大学医学院附属医院眼科,山东,青岛266003;海军401医院
2. 海军401医院
3. 复旦大学医学院
摘    要:
目的:研究N-甲基-D-天门冬氨酸受体(N-methyl-D-aspartate receptor,NMDAR)功能亚单位NMDAR1、NM-DAR2A在Wister大鼠视网膜缺血再灌注模型中的表达情况。方法:18只健康成年Wister大鼠分成6组,每组3只,都取其右眼行视神经周围血管结扎手术制备视网膜缺血再灌注模型,左眼作为对照组不行手术。60分钟后去除结扎缝线恢复血流,分别于再灌注后即刻、3、12、24、72、168小时处死大鼠,摘除眼球,做冰冻切片。用免疫组织化学方法观察NR1、NR2A在视网膜缺血再灌注后不同时刻的变化并进行图象分析及统计学处理。结果:(1)各实验组和对照组间及各实验组间NMDAR1的表达无统计学意义。(2)除即刻组外各实验组和对照组间及各实验组间NMDAR2A的表达均有统计学意义,从再灌注后3小时至168小时NMDR2A表达缓慢上升。结论:(1)NMDAR1与视网膜缺血再灌注损伤无关,不参与谷氨酸的兴奋性毒性作用。(2)NMDAR2A与视网膜缺血再灌注损伤有关,参与谷氨酸兴奋性毒性作用。

关 键 词:受体  N-甲基-D-天门冬氨酸  谷氨酸  受体  视网膜/损伤  视网膜/免疫学  动物  实验  大鼠  近交系
文章编号:1004-4469(2003)03-0170-05
修稿时间:2002-05-20

The expression of N-methyl-D-aspartate receptor(NMDAR)subunits NR1 and NR2A in the rat model of retinal ischemia reperfusion injury
DU Gai-ping. The expression of N-methyl-D-aspartate receptor(NMDAR)subunits NR1 and NR2A in the rat model of retinal ischemia reperfusion injury[J]. Ophthalmology in China, 2003, 12(3): 170-174
Authors:DU Gai-ping
Abstract:
Objective:To study the expression of N-methyl-D-aspartate receptor(NMDAR) subunits NR1 and NR2A in the model of rat retina ischemia-reperfusion. Methods: Eighteen Wister rats were randomly classified into six groups. Eighteen right eyes were performed the surgery of the optic nerve ligation for 60 minutes,and the eighteen left eyes were taken as normal control group without surgery. The rats were sarcrified immediately,3 hours, 12 hours,24 hours,72 hours and 168 hours after 60 minutes of ischemia. The rat eyes were nucleated and sectioned into 10 - 12 fan thickness slices on cryostat. The changes of NR1 and NR2A in the different groups by immunocytochemical technology were observed and image analysis was performed. Results:Between control group and experiment group, and among all experiment groups, the expression of NR1 was no significant difference, but the NR2A was statistic different except the immediate group. The expression of NR2A was gradually increased from 3 hours to 168 hours after ischemia-reperfusion injury. Conclusions:NR1 has no relation with the exciting toxic function of glutamate.but the NR2A has a relation with it.
Keywords:receptors   N-methyl-D-aspartate  glutamate  receptor  retina/injuries  retina/immunology  animal   laboratory  rats   in-brad strains
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