诱生型一氧化氮合酶及环氧化酶-2对氧诱导视网膜病变小鼠模型新生血管形成的影响  

Effect of inducible nitric oxide synthase or cyclooxygenase-2 on retinal neovascularization in oxygeninduced retinopathy mouse model

作　　者：贺涛[1] 邢怡桥[1] 艾明[1] 赵晓辉[1] 武犁[1] 叶美红[1] 彭斌[1] 

机构地区：[1]武汉大学人民医院眼科,430060

出　　处：《中华眼底病杂志》2008年第1期49-52,共4页Chinese Journal of Ocular Fundus Diseases

摘　　要：目的探讨环氧化酶2（COX-2）和诱生型一氧化氮合酶（iNOS）对氧诱导视网膜病变（OIR）小鼠模型视网膜新生血管形成的影响及其可能的作用机制。方法使用变化的氧浓度诱导小鼠的视网膜新生血管形成。用免疫组织化学、实时定量聚合酶链反应以及Western blotting检测COX-2、iNOS、基质金属蛋白酶-2（MMP2）和血管内皮生长因子（VEGF）在视网膜新生血管形成过程中的表达，并研究COX-2或iNOS抑制对视网膜新生血管形成的影响以及在此过程中MMP-2及VEGF的表达变化。结果COX2或iNOS抑制显著下调了VEGF和MMP-2的表达并减少了视网膜新生血管的形成。iNOS抑制减少了COX-2的表达，而COX-2抑制也同样下调了iNOS的表达。结论在OIR小鼠模型的视网膜新生血管形成过程中存在COX-2及iNOS的作用，它们对视网膜新生血管形成的影响可能通过调节VEGF和MMP-2的表达实现。Objective To investigate the effect of inducible nitric oxide synthase （iNOS） or cyclooxygenase-2 （COX-2） on retinal neovascularization and its possible mechanism in oxygen-induced retinopathy （OIR） mouse model. Methods Retinal neovascularization was induced by oxygen with different concentration. The expression of iNOS, COX-2, matrix metalloproteinases 2 （MMP-2） and vascular endothelial growth factor （VEGF） in the retinae of experimental animals were analyzed by immunohistochemistry, real-time polymerase chain reaction and western blotting technologies. Results The inhibition of COX-2 or iNOS obviously attenuated retinal neovascularization and decreased the expression of VEGF and MMP-2. The iNOS inhibition decreased COX-2 expression, and vice versa. Conclusions COX-2 and iNOS may play a role in retinal neovascularization in OIR mouse model, which may act by regulating the expression of VEGF and MMP-2.

关 键 词：视网膜病 早产儿/病因学 一氧化氮合酶/药物作用 环氧化酶2/药物作用 疾病模型 动物 

分 类 号：R686[医药卫生—骨科学]