中文摘要：

目的探讨改良钛支架人工角膜植入兔眼术后，角膜组织基质金属蛋白酶（MMP-2）及其抑制物（TIMP-2）的表达与角膜溶解的关系。方法实验研究。人工角膜支架改良：钛支架表面喷砂后用羟基磷灰石涂层（HA／SB—Ti）。将20只正常新西兰白兔分3组每组6只，其中A组、B组右眼角膜板层分别植入改良支架和对照支架（SB-Ti），C组仅做角膜板层切口，余2只为D组做空白对照。同样方法分组20只兔碱烧伤角膜模型，分别为E、F、G、H组。1个月、3个月后取材行免疫组织化学检测MMP-2、TIMP-2在不同组别的表达；为去除碱烧伤因素影响，另取24只正常动物模型改良支架植入后按时间分组，分别为2周组、1月组、3月组、5月组，每组6只，2只正常动物为空白对照组，用实时定量聚合酶链反应（RT—PCR）、免疫印迹法（Western blot）检测MMP-2、TIMP-2mRNA及蛋白的表达。5月组动物及2只碱烧伤模型动物，支架植入3个月后植入镜柱。实验数据采用t检验进行统计学分析。结果F组有一例出现角膜溶解的并发症。免疫组织化学检查结果：A与B及E与F比较MMP-2表达有统计学意义（t=12．05，2．93，12．00，3．78；P〈0．05）。于2周、1个月、3个月、5个月取材后，做RT．PCR、Westernblot检测，MMP-2mRNA及MMP-2蛋白表达从支架植入开始升高，1个月达到高峰，然后下降，仅2周与3个月MMP-2蛋白表达比较无统计学意义（t=2．104，P〉0．05）。而TIMP-2mRNA及TIMP-2蛋白表达在支架植入后有波动，然后逐渐升高，TIMP-2 mRNA除1个月与正常角膜组比较无统计学意义（t=1．878，P=0．0972）。结论改良后的人工角膜由于生物活性提高抑制了MMP-2的过度表达，MMP-2、TIMP-2表达随时问的变化规律可能为临床治疗并发症提供新的方法.

英文摘要：

Objectives To investigate the expression of matrix metalloproteinase-2 （MMP-2） and Tissue inhibior of matrix metalloproteinase-2 （ TIMP-2 ） in rabbit corneas implanted with modified titanium skirt of keratoprosthesis in order to explore the potential roles. Methods A total of 20 New Zealand white rabbits with corneal alkali burn in right eye rabbit corneas were divided into three groups. There were 6 animals in each group. Skirt of hydroxyapatite/Sandblast-Titanium and Sandblast-Titanium were inserted into the corneal stroma of rabbits in group A and group B. The group C did not insert skirt as surgical control. 2 rabbits were as normal control D group. A total of 20 New Zealand white rabbits were divided into four groups with the same way. The expression of MMP-2 and TIMP-2 was determined by immunohistochemistry at 1 month, 3 months. The expression of MMP-2 and TIMP-2 mRNA level was determined by real time-polymerase chain reaction, and its protein level was determined by western blot. The optical cylinder was implanted to rabbit corneas, which were implanted with modified titanium skirt after 3 months. Results There was one case of corneal dissolution being found in group F. MMP-2 and TIMP-2 immunoreactivities were expressed in the normal corneas, predominantly in the corneal epithelium. After injury, immunoreactivities of both MMP-2 and TIMP-2 were increased notably in the healing corneal epithelium, infiltrating inflammatory cells, stromal fibroblasts and in growing vascular endothelial cells. The expression of MMP-2 was lower in group A and E than that in group B and F after 1 month and 3 months （t = 12. 05,2. 93, 12. 006,3. 781 ,P 〈 0. 05 ）. The Western boh revealed no significant differences of MMP-2 mRNA between group 3 months and 2 weeks （ t = 2. 104, P 〉 0. 05 ） ; MMP-2 immunoreactivities were absent or lowly expressed predominantly in the corneal epithelium of normal corneas. The expression of MMP-2, TIMP-2 mRNA level was paralled that of protein level. Conclusions The expression of