MMPs抑制剂GM6001干预外伤性PVR的超微结构观察  

Ultramicrostructure of retina with traumatic proliferative vitreoretinopathy after Timps-GM6001 intervention

作　　者：徐国兴[1] 吴雅冰[1] 谢茂松[1] 

机构地区：[1]福建医科大学附属第一医院福建省眼科研究所,福州350005

出　　处：《眼科研究》2008年第12期904-907,共4页Chinese Ophthalmic Research

基　　金：卫生部科研基金项目(WKJ2005-2-013);福建省自然科学科研基金项目(C0510015);福建医科大学教授发展基金课题(2006-js6033)资助

摘　　要：目的观察基质金属蛋白酶(MMPs)抑制剂GM6001干预外伤性增生性玻璃体视网膜病变(PVR)视网膜超微结构的改变。方法取SD大鼠108只随机分为实验对照组36只、外伤性PVR组36只和GM6001干预组36只,应用透射电镜观察视网膜超微结构改变。结果外伤性PVR组大鼠视网膜光感受器细胞、视网膜色素上皮(RPE)细胞、视网膜内外屏障受损,而应用GM6001干预组视网膜光感受器细胞外节膜盘结构尚清晰;RPE基底部质膜内褶较外伤性PVR组多,胞质中含大量线粒体、吞饮小泡和滑面内质网,部分线粒体嵴脱失;细胞连接清晰、规则。结论MMPs抑制剂GM6001干预可保护视网膜组织结构,GM6001在干预外伤性PVR的发生发展中起重要作用。Objective GM6001 is an inhibitor of matrix metalloproteinases（MMPs）. It has been determined that GM6001 can protect retina fi＇om the vitreoretinopathy induced by the overexpression of MMPs. This study was to observe the uhramierostructure of retina with traumatic proliferative vitreoretinopathy（PVR） and the effects of Timps-GM6001 on traumatic PVR. Methods 108 SD rats were divided randomly into 3 groups at average. 20μL normal saline solution was intravitreously injected in the left eyes in the model group, and traumatic PVR was induced through intravitreously injection of 20μL serum of SD rats blood in PVR group. 20 μL Timps-GM6001 was injected into rat vitreous in the eyes with traumatic PVR eyes after 12 hours. The right eyes were as control group. Retinal uhramierostrueture was revealed under the the transmission electron microscope. Results The proliferative membrane of vitreoretinopathy and retinal tear were seen by the photography. The damage of the retinal photoreeeptor cells,retinal pigment epithelium and retinal inner and outer barriers was found under the transmission electron microscope in traumatic PVR group. However, in GM6001 injection group, the membranous discs of outer segment of retinal photoreeepter cells were still clear. Plenty of chondriosome, pinoeytosis bullules and smooth endoplasmie reticulum in the cytoplasm could be seen, but some of the eristae in the chondriosome were absent. The intercellular junction was clear and regular,and the plasma membrane infoldings of the basilar part of retinal pigment epithelium were more in GM6001 group than in traumatic PVR group. Conclusion GM6001 plays an important role in interfering the course of traumatic PVR through protecting retinal uhramicrostructure.

关 键 词：外伤性增生性玻璃体视网膜病变 GM6001 超微结构 视网膜 

分 类 号：R774.1[医药卫生—眼科]