摘要
目的观察血管内皮细胞生长因子受体嵌合蛋白对缺血性视网膜病变小鼠模型的视网膜新生血管化的抑制作用。方法以高浓度氧诱导C57BL/6J小鼠建立视网膜缺血性病变动物模型,应用不同浓度VEGF受体嵌合蛋白进行玻璃体腔内注射,在组织切片上计数和比较正常和实验条件下以及不同浓度药物注射后视网膜新生血管芽细胞核数。结果视网膜新生血管芽细胞核数:正常对照组(1.06±2.08)个;高氧对照组(128·69±46.07)个,flt-1小剂量治疗组(85.31±35.46)个,flt-1大剂量治疗组(63.13±24.40)个,flk-1小剂量治疗组(90·50±38.03)个,flk-1大剂量治疗组(67.13±23.13)个,flt-1+flk-1治疗组(42.69±17.75)个。各用药组与高氧对照组间均有显著性差异,P<0.05。结论血管内皮细胞生长因子受体嵌合蛋白能有效抑制视网膜新生血管的增生。
Objective To observe the inhibitive effects of vascular endothelial growth factor （VEGF） receptor chimeric proteins on retinal neovascularization in ischemia-induced mice model. Methods Ischemic retinopathy mice model were established by hyperoxia-induced. Intravitreal injections were performed with different concentrations of VEGF fit-1 or/and flk-1 chimeric proteins or NS. The nuclei of new vessel buds extending from the retina into the vitreous in different groups were counted and compared. sults The number of new vessel buds in control group was （1.06 ± 2.08）, in hyperoxia control group was （ 128.69 ± 46.07）, in small-dosage fit-1 group was （85.31 ± 35.46）, in large-dosage fit-1 group was （63.13 ±24.40）, in small-dosage flk-1 group was （90.50 ± 38.03）, in large-dosage flk-1 group was （67.13 ±23.13）, in fit-1 and flk-1 group was （42.69 ±17.75）. There were significant differences between every treated group and hyperoxta control group（P〈0.01 ）. Conclusion VEGF neutralizing chimeric proteins can inhibit the proliferation of retinal neovascularization effectively.
出处
《眼科新进展》
CAS
2006年第6期432-435,共4页
Recent Advances in Ophthalmology
关键词
视网膜新生血管化
内皮生长因子
受体嵌合蛋白
retinal neovascularlzation
endothelial growth factor
neutralizing chimeric proteins
