大鼠角膜新生血管模型中基质金属蛋白酶-2及其抑制物的表达

Expression of matrix metalloproteinase-2 and its inhibitor in rat corneal neovascularization model

目的 探讨大鼠角膜碱烧伤后基质金属蛋白酶-2（MMP-2）及其组织型抑制剂（TIMP-2）在角膜中的表达和意义。方法 采用碱烧伤大鼠角膜建立角膜新生血管动物模型;应用免疫组织化学技术检测MMP-2及TIMP-2在角膜新生血管模型不同阶段的表达和变化。结果 实验鼠于伤后3～4天开始形成大量新生血管,可见炎性细胞浸润,伤后14～21天新生血管和炎性细胞均明显减少。免疫组化显示MMP-2于伤后1天表达开始升高,3天达最高,以后逐渐下降。而TIMP-2则于早期变化不明显,7天表达开始升高,14天达高峰。结论 大鼠角膜新生血管形成早期MMP-2活性增高,继而TIMP-2分泌增多,MMP-2活性受抑,基底膜降解受阻,新生血管延伸停滞。

Objective To investigate the expression of matrix metalloproteinase-2 (MMP-2) and its tissue inhibitor in rat eornea after cautery with alkali. Methods Corneal neovaseularization was induced by cautery with alkali in Wislar rats. The expression of MMP-2 and TIMP-2 was studied by immunohistochemislry, and the results were analyzed by picture quantitative analysis technique. Results Significant neovaseularization appeared in rat cornea on the 3rd day after cautery with alkali. Also, the inflammatory reaction was observed. The neovaseularization and the inflammatory cell decreased from the 14th day to the 21th day. By immanohistochemistry, increased expression of MMP-2 was found on the 1st day . being highest on the 3rd day , then decreased slowly. However, the changes of TIMP-2 were not obvious in the early phrase,and the increased expression of TIMP-2 was found on the 7th day,with the highest levels seen on the 14th day. Conclusions The activity of MMP-2 increase in the early stage of rat corneal neovascularization model, then is inhibited by the increased expression of TIMP-2. The degradation of ECM is disrupted , and neovaseularization is stopped.