血管内皮生长因子及其受体在DR患者玻璃体中的表达
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深圳市福田区卫生公益性科研项目(No. FTWS201366)


Expression of vascular endothelial cell growth factor and its receptors in vitreous of patients with diabetic retinopathy
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Health and Public Welfare Scientific Research Project of Futian District, Shenzhen(No. FTWS201366)

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    摘要:

    目的:观察血管内皮生长因子(vascular endothelial cell growth factor, VEGF)及其受体在糖尿病视网膜病变(diabetic retinopathy, DR)患者玻璃体中的表达,探讨其在DR发生发展中的作用。

    方法:对13例16眼DR患者和15例15眼健康人,采用免疫组织化学法检测其玻璃体新生血管膜的VEGF及其受体(fms-样酪氨酸激酶, Flt-1和含激酶插入区受体, KDR)表达情况,同时采用酶联免疫吸附法(ELISA)检测DR患者玻璃体中VEGF、Flt-1和KDR的浓度。

    结果:免疫组织化学染色显示,DR患者玻璃体血管膜中VEGF、Flt-1和KDR高度表达,玻璃体中VEGF、Flt-1和KDR浓度明显高于对照组(P<0.05或P<0.01)。

    结论:VEGF及其受体Flt-1、KDR在DR患者玻璃体中高度表达,与DR患者的微血管生成关系密切,提示VEGF及其受体在DR的发生发展中起重要作用。

    Abstract:

    AIM:To investigate the expression of vascular endothelial cell growth factor(VEGF)and its receptors in vitreous of patients with diabetic retinopathy(DR), and to discuss its role in the development of DR.

    METHODS: Selected 13 patients(16 eyes)with DR and 15 healthy people(15 eyes), the expression of VEGF and its receptors(fms-like tyrosine kinase-1, Flt-1 and kinase insert domain containing receptor, KDR)were evaluated by immunohistochemistry in vitreous. The levels of VEGF, the Flt-1 and KDR in vitreous of patients with DR were examined with enzyme linked immunosorbent assay(ELISA).

    RESULTS: Immunohistochemical staining showed that the expression of VEGF, Flt-1 and KDR in vitreous vessel membrane of patients with DR was increased significantly. And the levels of VEGF, Flt-1 and KDR in vitreous of patients with DR were obviously higher than that in the control group(P<0.05 or P<0.01).

    CONCLUSION: VEGF, Flt-1 and KDR were widely expressed in vitreous of patients with DR, and were positively related to micro-angiogenesis of DR patients. It proved that VEGF and its receptors played important roles in the occurrence and development of DR.

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利焕廉,周金文,左炜.血管内皮生长因子及其受体在DR患者玻璃体中的表达.国际眼科杂志, 2014,14(9):1587-1589.

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  • 收稿日期:2014-04-13
  • 最后修改日期:2014-07-29
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  • 在线发布日期: 2014-08-19
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