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儿茶酚胺在大鼠早产儿视网膜病变实验模型中病理性视网膜新生血管形成中的作用

The Role of Catecholamines in the Development of Pathological Retina Neovascularization in an Experimental Model of Retinopathy of Prematurity in Rats.

作者信息

Katargina L A, Osipova N A, Panova A Y, Petrovskaya A V, Nikishina Y O, Murtazina A R, Ugrumov M V

机构信息

Moscow Helmholtz Institute of Ophthalmology, Ministry of Health of the Russian Federation, 103064, Moscow, Russia.

Koltzov Institute of Developmental Biology, Russian Academy of Sciences, 119334, Moscow, Russia.

出版信息

Dokl Biochem Biophys. 2019 Nov;489(1):373-376. doi: 10.1134/S160767291906005X. Epub 2020 Mar 4.

DOI:10.1134/S160767291906005X
PMID:32130603
Abstract

This work is dedicated to proving our hypothesis that catecholamines and their metabolites play a crucial role in the development of retinopathy of prematurity, which leads to progressive uncontrollable vascularization in the retina, leading to blindness. The study was performed in an animal model of retinopathy of prematurity, which was achieved by hyperoxygenation in rats on postnatal days 7, 14, 21, and 30. The content of catecholamines and their metabolites in the retina of rats was determined by high performance liquid chromatography with electrochemical detection. It was shown that, in the rats with retinopathy, the content of L-DOPA on days 21 and 30 was decreased as compared to the control, whereas the content of noradrenaline on day 14 life increased compared to the control. However, we did not observe changes in the content of dopamine in the experimental animals relative to the control in any period studied. Given the published data on the involvement of catecholamines in the regulation of vasculogenesis in the retina in normal state, our data on the changes in the catecholamine metabolism in the retina in the model of retinopathy of prematurity can be regarded as evidence of the important role of catecholamines in the pathogenesis of this severe disease.

摘要

这项工作致力于证明我们的假设,即儿茶酚胺及其代谢产物在早产儿视网膜病变的发展中起关键作用,该病变会导致视网膜中不可控制的血管增生,进而导致失明。该研究在早产儿视网膜病变的动物模型中进行,通过在出生后第7、14、21和30天对大鼠进行高氧处理来实现。大鼠视网膜中儿茶酚胺及其代谢产物的含量通过高效液相色谱电化学检测法测定。结果表明,患有视网膜病变的大鼠在第21天和第30天时,左旋多巴的含量与对照组相比有所降低,而在出生后第14天时,去甲肾上腺素的含量与对照组相比有所增加。然而,在任何研究时期,我们都未观察到实验动物中多巴胺含量相对于对照组有变化。鉴于已发表的关于儿茶酚胺在正常状态下参与视网膜血管生成调节的数据,我们关于早产儿视网膜病变模型中视网膜儿茶酚胺代谢变化的数据可被视为儿茶酚胺在这种严重疾病发病机制中起重要作用的证据。

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本文引用的文献

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Vulnerability of Dopaminergic Amacrine Cells to Chronic Ischemia in a Mouse Model of Oxygen-Induced Retinopathy.在氧诱导性视网膜病变小鼠模型中多巴胺能无长突细胞对慢性缺血的易损性
Invest Ophthalmol Vis Sci. 2016 Jun 1;57(7):3047-57. doi: 10.1167/iovs.16-19346.
2
Protective effects of β1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy.β1/2肾上腺素能受体缺失在氧诱导性视网膜病变模型中的保护作用
Invest Ophthalmol Vis Sci. 2014 Dec 11;56(1):59-73. doi: 10.1167/iovs.14-15263.
3
The rat with oxygen-induced retinopathy is myopic with low retinal dopamine.
氧诱导视网膜病变大鼠近视且视网膜多巴胺含量低。
Invest Ophthalmol Vis Sci. 2013 Dec 19;54(13):8275-84. doi: 10.1167/iovs.13-12544.
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Oral propranolol versus placebo for retinopathy of prematurity: a pilot, randomised, double-blind prospective study.口服普萘洛尔与安慰剂治疗早产儿视网膜病变:一项前瞻性、随机、双盲试点研究。
Arch Dis Child. 2013 Jul;98(7):565-7. doi: 10.1136/archdischild-2013-303951. Epub 2013 Apr 30.
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PEDF and VEGF-A output from human retinal pigment epithelial cells grown on novel microcarriers.在新型微载体上生长的人视网膜色素上皮细胞分泌的色素上皮衍生因子(PEDF)和血管内皮生长因子A(VEGF-A)
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Future Oncol. 2010 Dec;6(12):1863-81. doi: 10.2217/fon.10.142.
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Angiogenesis: update 2005.血管生成:2005年最新进展
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Rat retinal dopaminergic neurons: differential maturation of somatodendritic and axonal compartments.大鼠视网膜多巴胺能神经元:胞体树突和轴突部分的差异成熟
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