摘要
目的:观察可溶性Tie2融合蛋白(soluble Tie2 fusion pro-tein,sTie-Fc)对视网膜血管新生(retinal neovascularization,RNV)的抑制作用,同时分析其对缺血性视网膜病变的影响。方法:将生后7d的C57BL/6幼鼠置于高氧箱中饲养5d取回至正常空气环境诱导RNV模型,生后12d和14d选取一眼玻璃体腔注入人sTie-Fc0.67μg,对侧眼在相同时点注入人IgG作为对照。生后17d处死动物行视网膜铺片和免疫组织化学染色检查,测量视网膜血管无灌注区的面积,计数RNV内皮细胞核数目,定量分析sTie-Fc对于缺血性视网膜病变以及实验性RNV形成的影响。结果:对照组和实验组均成功建立了RNV模型,实验组RNV的形成受到抑制(P<0.05),同时sTie-Fc也加重了RNV模型的缺血过程(P<0.05)。结论:sTie-Fc可以抑制实验性RNV的发展,提示拮抗Tie2可能成为治疗RNV有效的生物学方法之一,其可能加重缺血性视网膜病变的潜在副作用需进一步探讨。
AIM： To investigate the effects of neutralizing Tie2 on retinal neovascularization （RNV） and ischemic retinopathy in the mouse model of oxygen-induced retinopathy （OIR）.
METHODS： C57BL/6 mice at postnatal day 7 were exposed to 750mL/L oxygen for 5 days and allowed to recover in room air to induce RNV. At the 12th and 14th day, the animals were intravitreally injected with 0.67μg soluble Tie2 fusion protein （sTie-Fc）. Retinal fluorescein angiography and immunohistochemical staining were used to assess the development of ischemic retinopathy and experimental RNV quantitatively at the 17th day, by measuring the area of vascular obliteration and counting the number of preretinal nuclei. RESULTS： sTie-Fc significantly inhibited the formation of RNV （P〈 0.05） and aggravated the ischemia （ P 〈 0.05） compared with control mice.
CONCLUSION ： Our findings suggest that Tie2 may be a promising potential target for antiangiogenesis therapy for RNV. Further research is needed to decrease the undesirable effect of inhibiting retinal revascularization.
出处
《国际眼科杂志》
CAS
2008年第3期502-504,共3页
International Eye Science
