摘要
目的探讨角膜烧伤后基质金属蛋白酶9(MMP9)及其组织型抑制剂(tissueinhibitorofmetallopoteinase1,TIMP1)在小鼠角膜中的表达及意义。方法采用1mol·L-1氢氧化钠溶液烧伤昆明小鼠角膜,建立角膜碱烧伤动物模型;用免疫组织化学染色方法和计算机图像分析系统检测小鼠角膜烧伤后不同时间点MMP9及TIMP1在角膜中的分布及其积分吸光度(A)值。结果小鼠角膜碱烧伤后第2d炎性细胞增多,第7d炎症达到高峰,21d后基本消失。小鼠角膜上皮层、基底膜、以及基质层中大量炎性细胞和新生血管内皮细胞均有MMP及TIMP1表达。角膜中MMP9在第2d出现表达,第7d达高峰,以后逐渐降低;TIMP1开始表达不明显,第7d出现表达,14d达高峰,以后逐渐降低。结论小鼠碱烧伤模型炎症早期MMP9活性增高,继而TIMP1分泌增多,MMP9活性受抑,炎症减轻。提示MMP9可能是参与碱烧伤角膜溃疡形成、角膜融解及纤维化的重要调控因子,而TIMP1则在炎症的抑制过程中发挥了重要作用。
Objective To study the expression and role of matrix metalloproteinase 9（MMP-9） and its tissue inhibitor（TIMP-1 ） in KM mice cornea after cautery with alkali.Methods The model of corneal alkali burn was established in KM mice with lmol· L^-1 sodium hydroxide. The expression of MMP-9 and TIMP-1 were detected by immunohistochemistry, and the results were analyzed by comaputer medical image analysis system at different time points.Results In the early stage of burn, the inflammatory cells in cornea was observed at the 2nd day, peaked at the 7th day,and disappeared at the 21th day.MMP-9 and TIMP-1 were expressed in the epithelial cells,basement membrane, and exudated inflammatory ceUs and vascular endothelial cells in stroma, The level of MMP-9 elevated at the 2nd day,peaked at the 7th day,dropped gradually afterwords. TIMP-1 was expressed at the 7th day,reached peaks at the 14th day,and decreased gradually to the base line level.Conclusion The activity of MMP-9 increased in the early stage of alkaliburned mouse model. Later TIMP-1 was secreted and increased to inhibit the inflammation by restraining the activity of MMP-9. It＇ s suggest that MMP-9 take an active part in the formation of corneal ulcer, cornea melting and fibrosis, and TIMP-1 play an important role in inhibiting the inflammation.
出处
《眼科新进展》
CAS
2005年第4期309-311,共3页
Recent Advances in Ophthalmology
基金
国家教育部留学人员启动基金(编号:2003406)~~
