外伤性PVR大鼠视网膜中MMP-9、TIMP-1的表达及意义  

Expression of MMP-9,TIMP-1 on the traumatic PVR retina of SD rats

作　　者：徐国兴[1] 冯春燕[1] 

机构地区：[1]福建医科大学附属第一医院眼科,福建省眼科研究所,中国福建省福州市350005

出　　处：《国际眼科杂志》2008年第10期1997-2000,共4页International Eye Science

基　　金：福建省自然科学基金(No.C0510015)~~

摘　　要：目的:为研究外伤性PVR和外伤后应用GM6001干预大鼠视网膜组织MMP-9及TIMP-1、在不同病程中的表达变化。方法:360只SD大鼠随机分为正常对照组、外伤性PVR组和外伤后应用GM6001组。正常对照组玻璃体腔内注射生理盐水;外伤性PVR组玻璃体腔内注射PRP血浆制成外伤性PVR大鼠动物模型;外伤后应用GM6001组在外伤后12h玻璃体腔内注射GM6001。应用免疫组化染色方法分别于1,3,7,14,21,28d对各组大鼠视网膜组织MMP-9及TIMP-1的表达检测。结果:免疫组化结果示MMP-9、TIMP-1蛋白均主要表达于视锥视杆层、视网膜内外网状层、神经纤维层。MMP-9在正常对照组、外伤后应用GM6001组的各个亚组微弱表达。MMP-9在外伤性PVR组1,3,7d显著表达,与正常对照组和外伤后应用GM6001组的差异有显著性(P(0.01),随着病程的延长,MMP-9的表达呈进行性减弱的趋势;TIMP-1在外伤性PVR组与外伤后应用GM6001组的各个亚组均有明显表达,与正常对照组的差异均有显著性(P(0.01)。MMP-9/TIMP-1比率在外伤性PVR组1,3,7d增高,与正常对照组和外伤后应用GM6001组的差异均有显著性(P(0.05)。结论:MMP-9、TIMP-1参与了PVR发生发展的病理过程,MMP-9/TIMP-1比率增高促进PVR发生发展的进程。人工合成基质金属蛋白酶抑制剂GM6001可促进MMP-9/TIMP-1动态平衡的重新建立,从而在外伤性PVR的防治中起重要作用。AIM ： To investigate the expression of MMP-9 and TIMP-1 during the course of traumatic PVR treated with GM6001 and without GM6001, to explore the potential role of MMP-9 and TIMP-1 during the course of traumatic PVR and to evaluate the effect of GM6001 on traumatic PVR prevention and treatment. METHODS： Totally 360 SD rats were divided randomly into three groups： normal control group, the traumatic PVR group, the traumatic PVR treated with GM6001 group. The normal control group was intravitreous injected with normal saline. The traumatic PVR group was intravitreous injected with the PRP. The traumatic PVR treated with GM6001 group was intravitreous injected with the PRP and GM6001. The expression of MMP-9 and TIMP-1 were qualitative and semiquantitative analyzed with immunohistochemistry on day 1,3, 7, 14, 21 and 28. RESULTS： Immunohistochemistry showed that the expression of MMP-9 and TIMP-1 were mainly located in the photoreceptor cells layer, out plexiform layer, inner plexiform layer and nerve fiber layer. The expression of MMP-9 in the normal group and the traumatic PVR treated with GM6001 group were weak at all time. The expression of MMP-9 in the traumatic PVR group was strong at day 1, 3 and 7. The differences were statistically significant as compared with the normal group and the traumatic PVR treated with GM6001 group （ P 〈 0.01 ）. The expression of MMP-9 in the traumatic PVR group decreased at the following time. The expression of TIMP-1 in the traumatic PVR group and the traumatic PVR treated with GM6001 group were strong at all time. The differences were statistically significant as compared with the normal group （P〈 0.01 ）. The rate of MMP-9/TIMP-1 in the traumatic PVR group increased at day 1, 3 and 7. The differences were statistically significant as compared with the normal group and the traumatic PVR treated with GM6001 group （P〈0.05）. CONCLUSION ： MMP-9 and TIMP-1 involve in the course of traumatic PVR. The higher rate of MMP-9/TIMP-1 promotes the course of traum

关 键 词：基质金属蛋白酶-9 基质金属蛋白酶抑制剂-1 GM6001 外伤性增生性玻璃体视网膜病变 免疫组化 

分 类 号：R779.1[医药卫生—眼科]