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机构地区:[1]福建医科大学附属第二医院,中国福建省福州市350005 [2]福建医科大学附属第一医院,中国福建省福州市350005
出 处:《国际眼科杂志》2008年第11期2195-2198,共4页International Eye Science
基 金:中国卫生部科研基金资助项目(No.WKJ2005-2-013);福建省自然科学科研基金项目(No.C0510015);福建医科大学教授发展基金课题(No.2006-js6033)~~
摘 要:目的:观察外伤性PVR大鼠和外伤后应用人工合成基质金属蛋白酶抑制剂(GM6001)中大鼠视网膜组织MMP-1、MMP-3及TIMP-1在不同病程中的表达变化。方法:将180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。应用免疫组化法在不同时间对各组大鼠视网膜组织MMP-1、MMP-3及TIMP-1的表达进行定性、定位、半定量检测。结果:1)MMP-1、MMP-3、TIMP-1主要表达于视网膜组织的视锥视杆层、视网膜外网状层、视网膜内网状层、神经纤维层。2)各个亚组在正常对照组、外伤后应用GM6001组MMP-1、MMP-3微弱表达。3)MMP-3在外伤性PVR组1,3,7d显著表达,MMP-1在外伤性PVR组3,7,14d显著表达(P<0.05)。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(P<0.01)。MMP-3/TIMP-1的比率在外伤性PVR组1,3,7d增高(P<0.05)。MMP-1/TIMP-1的比率在外伤性PVR组3,7,14d增高(P<0.05)。结论:MMP-1、MMP-3与PVR形成的病理过程有关,TIMP-1与二者特异性结合抑制其活性。GM6001通过调节MMP-1/TIMP-1和MMP-3/TIMP-1达到平衡,能抑制PVR的发生和发展,干预PVR的发展进程。AIM- To investigate the expression of MMP-1, MMP-3 and TIMP-1 during the course of traumatic PVR treated with GM6001 and without GM6001. METHODS: Totally 180 SD rats were divided randomly into three groups: normal control group, the traumatic PVR group, the traumatic PVR treated with GM6001 group. The expression of MMP-1, MMP-3 and TIMP-1 were qualitative and semiquantitative analysised with immunohistochemistry at different times. RESULTS. 1 ) Immunohistochemistry showed that the expression of MMP-1, MMP-3 and TIMP-1 were mainly located in the photoreceptor cells layer, out plexiform layer, inner plexiform layer and nerve fiber layer. 2) The expression of MMP-1 and MMP-3 in the normal group and the traumatic PVR treated with GM6001 group were weak at all time. 3) The expression of MMP-3 in the traumatic PVR group was strong at day 1, 3 and 7. The expression of MMP-3 in the traumatic PVR group was strong at day 3, 7 and 14 (P〈 0. 05). The expression of TIMP-1 in the traumatic PVR group and the traumatic PVR treated with GM6001 group were strong at all time (P〈0.01). The rate of MMP-3/TIMP-1 in the traumatic PVR group increased at day 1,3 and 7 (P〈0.05). The rate of MMP-1/TIMP-1 in the traumatic PVR group increased at day 3, 7 and 14 (P〈0.05). CONCLUSION: MMP-1 and MMP-3 play key role in the course of traumatic PVR. TIMP-1 binds specifitly to MMP-1 and MMP-3 and suppressed their activity. GM6001 plays an important role in the course of traumatic PVR prevention and treatment by regulating the rate of MMP-1/ TIMP-1 and MMP-3/TIMP-1.
关 键 词:基质金属蛋白酶-1 基质金属蛋白酶-3 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
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