摘要
目的观察MK-801对低强度激光视网膜照射后谷氨酸受体(NMDAR)表达的拮抗作用,探讨MK-801治疗激光视网膜损伤的可能机制。方法用氦氖激光造成大鼠视网膜损伤模型,照后即刻肌注MK-801(2 mg/kg),通过免疫组化和原位杂交等方法,观察MK-801对激光照射后视网膜细胞中NMDAR蛋白和mRNA表达变化的影响。结果免疫组化和原位杂交的结果显示,激光照射后视网膜中NMDAR的表达显著增加,与视网膜的损伤程度相一致,照后给予MK-801可明显地减少视网膜中NMDAR的表达。结论谷氨酸受体的高表达可能是激光致眼损伤的机制之一,而MK-801可以通过抑制其表达来拮抗低强度激光所导致的视网膜损伤。
Objective To observe the effect of MK-801 on the expression of glutamate receptor after laser irradiation and to explore the possible mechanism of therapeutic effect of MK-801 on laser-induced retina injury. Methods After irradiation with low power He-Ne laser for 15 mins, Wistar rats immediately received an intramuscular injection of MK-801. The curative effects of MK-801 were observed by detection of the expression of glutamate receptor （NMDAR） in the rat retina. Results Laser irradiation induced a remarkable increase of NMDAR expression which corresponded with the retina injury process. However, the level of NMDAR expression decreased dramatically after administration of MK-801. Conclusion High expression of NMDAR is a possible mechanism through which laser cause experimental retinal injury. MK-801 showed the neuroprotective effect due to its blocking effect on NMDAR expression.
出处
《首都公共卫生》
2014年第2期56-59,共4页
Capital Journal of Public Health
基金
国家自然科学基金资助项目(81000685
81072239)
北京市自然科学基金资助项目(7142124)
