MMP-2、TIMP-2在外伤性PVR大鼠视网膜中的表达

Expression of MMP-2 and TIMP-2 in the Traumatic PVR Retina of SD Rats.

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-2、TIMP-2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、28天对各组大鼠视网膜组织MMP-2、TIMP-2的表达检测。结果1.免疫组化结果示MMP-2、TIMP-2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。2.MMP-2在正常对照组、外伤后应用GM6001组的各个亚组微弱表达。MMP-2在外伤性PVR组14、21、28天表达增强,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-2的表达呈进行性增高的趋势。TIMP-2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)。3.MMP-2/TIMP-2比率外伤性PVR组14、21、28天增高,与正常对照组和外伤后应用GM6001组的差异有显著性(均P<0.05)。结论MMP-2、TIMP-2参与了PVR发生发展的病理过程,MMP-2/TIMP-2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-2/TIMP-2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。

Objective To investigate the expression of MMP - 2 and TIMP - 2 during the course of traumatic PVR treated with GM6001 and without GM6001 , and to explore the potential role of MMP -2 and TIMP -2 during the course of traumatic PVR and to eval uate the effect of GM6001 on traumatic PVR prevention and treatment. Methods 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 - 2 and TIMP - 2 were qualitativly and semiquantitativly analyzed with immunohistochemistry on day 1, 3, 7, 14, 21 and 28. Results 1. The results of immunohistochemistry showed that the expression of MMP - 2, TIMP - 2 was mainly located in the photoreceptor cells layer, out plexiform layer, inner plexiform layer and nerve fiber layer. 2. The expression of MMP -2 in the normal group and the traumatic PVR treated with GM6001 group was weak at all time. The differences were statistical significance as compared with the normal group and the traumatic PVR treated with GM6001 group （ P 〈 0.01 ）. The expression of MMP - 2 in the traumatic PVR group was strong at day 14,21and 28. The differences were statistical significance as compared with the normal group and the traumatic PVR treated with GM6001 group was （P 〈0. 01 ）. The expression of MMP -2 in the traumatic PVR group decreased at the following time. The expression of TIMP -2 in the traumatic PVR group and the traumatic PVR treated with GM6001 group strong at all time. The differences were statistical significance as compared with the normal group （P 〈0.01 ）. 3. The rate of MMP- 2/TIMP -2 in the traumatic PVR group increased at day 14, 21 and 28. The differences were statistical significance as compared with the normal group and the traumatic PVR treated with GM6001 group （P 〈0. 05）. Conclusion MMP -2 and TIMP -2 participate in the course of traumatic PVR. The higher rate of MMP -2/TIMP -2 promotes the course of traumatic PVR. GM6001 plays an important role in the course of traumatic PVR prevention and treatment by regulating the rate of MMP- 2/TIMP-2.