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[内皮抑素在氧诱导视网膜病变小鼠模型视网膜中的表达及作用]

[Expression and role of endostatin in the retina of oxygen-induced retinopathy mouse model].

作者信息

Zhang Mei-xia, Zhang Jun-jun, Yan Mi

机构信息

The West China Ophthalmic Center, West China Hospital, Sichuan University, Chengdu 610041, China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2006 Jul;37(4):614-7.

PMID:16909615
Abstract

OBJECTIVE

To investigate the effect of endostatin on the pathogenesis and development of retinal neovascula animal model of oxygen-induced retinopathy.

METHODS

The animal model of oxygen-induced retinopathy was made by subjecting postnatal mice to hyperoxic conditions (5 days) followed by normoxic conditions. Retinal angiogram was taken by using high molecular weight fluorescein-dextran. The degree of hyperoxia-induced neovascularization in serial paraffin cross-sections was quantified by counting the number of vascular cell nuclei on vitreal side of the internal limiting membrane. The expression of ES and VEGF in the oxygen-induced retina was observed by immunohistochemistry.

RESULTS

We successfully constructed the oxygen-induced retinopathy mouse model. FITC-dextran retinal angiography indicated that hyperoxia could produce constriction of retinal vasculature and vaso-obliteration or irreversible closure of many capillary channels and eventually result in non-perfused area in the post-area of retina surrounding the optic disk. Relatively, hypoxia could lead to dilation and torsion of retinal vessels. There were averagely 22 neovascular nuclei per cross-section of eyes in the hyperoxia group and less than 3 nuclei per cross-section of eyes in the control group (P < 0.05). The expressions of ES and VEGF in the retina under hyperoxia were stronger than those under normoxia, expecially the expression of VEGF.

CONCLUSION

Taking measures to up-regulate the expression of endogenetic endostatin may have the potential for effective treatment of retinal ischemic neovascularization.

摘要

目的

研究内皮抑素对氧诱导性视网膜病变动物模型视网膜新生血管形成及发展的影响。

方法

通过将出生后小鼠置于高氧环境(5天),随后再置于常氧环境,制备氧诱导性视网膜病变动物模型。使用高分子量荧光素-葡聚糖进行视网膜血管造影。通过计数内界膜玻璃体侧的血管细胞核数量,对连续石蜡切片中高氧诱导的新生血管形成程度进行量化。采用免疫组织化学法观察氧诱导视网膜中内皮抑素(ES)和血管内皮生长因子(VEGF)的表达。

结果

成功构建了氧诱导性视网膜病变小鼠模型。异硫氰酸荧光素-葡聚糖视网膜血管造影显示,高氧可导致视网膜血管收缩、血管闭塞或许多毛细血管通道不可逆性关闭,最终导致视盘周围视网膜后区出现无灌注区。相对而言,低氧可导致视网膜血管扩张和扭曲。高氧组每只眼的横切面平均有22个新生血管细胞核,对照组每只眼的横切面少于3个细胞核(P<0.05)。高氧条件下视网膜中ES和VEGF的表达高于常氧条件下,尤其是VEGF的表达。

结论

采取措施上调内源性内皮抑素的表达可能对视网膜缺血性新生血管形成具有有效的治疗潜力。

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Sichuan Da Xue Xue Bao Yi Xue Ban. 2006 Jul;37(4):614-7.
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