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基于年龄相关性眼病研究组(AREDS)的微量营养素对糖尿病大鼠视网膜病变和视网膜代谢异常的抑制作用。

Inhibition of retinopathy and retinal metabolic abnormalities in diabetic rats with AREDS-based micronutrients.

作者信息

Kowluru Renu A, Kanwar Mamta, Chan Pooi-See, Zhang Jiang Ping

机构信息

Kresge Eye Institute, Wayne State University, 4717 St Antoine, Detroit, MI 48201, USA.

出版信息

Arch Ophthalmol. 2008 Sep;126(9):1266-72. doi: 10.1001/archopht.126.9.1266.

Abstract

OBJECTIVES

To investigate whether the micronutrients that were shown to reduce the risk of development of age-related macular degeneration in the Age-Related Eye Disease Study (AREDS) can have the same effect on the development of diabetic retinopathy in rats, and to understand the possible mechanisms.

METHODS

Streptozotocin-induced diabetic rats received a powdered diet with or without supplemental micronutrients (ascorbic acid, vitamin E, beta-carotene, zinc, and copper). The retina was used after the rats had diabetes for 12 months to detect vascular histopathology and to measure the biochemical parameters and messenger RNA levels of the genes involved in oxidative and nitrative stress.

RESULTS

The AREDS-based micronutrients prevented a diabetes-induced increase in the number of retinal acellular capillaries. In the same rats, micronutrients inhibited increases in retinal oxidatively modified DNA and nitrotyrosine and decreases in manganese superoxide dismutase. Diabetes-induced alterations in the messenger RNA expression of mitochondrial electron transport complex III (coenzyme Q cytochrome-c reductase) and inducible nitric oxide synthase were also prevented.

CONCLUSION

Age-Related Eye Disease Study-based micronutrients inhibit the development of diabetic retinopathy in rodents by inhibiting oxidative and nitrative stress.

CLINICAL RELEVANCE

Micronutrients that slow down the onset and progression of age-related macular degeneration have the potential to inhibit the development of diabetic retinopathy.

摘要

目的

研究在年龄相关性眼病研究(AREDS)中显示可降低年龄相关性黄斑变性发生风险的微量营养素,对大鼠糖尿病视网膜病变的发生是否具有相同作用,并了解其可能机制。

方法

用链脲佐菌素诱导糖尿病大鼠,给予含或不含微量营养素补充剂(抗坏血酸、维生素E、β-胡萝卜素、锌和铜)的粉状饮食。大鼠患糖尿病12个月后,取视网膜检测血管组织病理学,并测量参与氧化应激和硝化应激的基因的生化参数及信使核糖核酸水平。

结果

基于AREDS的微量营养素可防止糖尿病诱导的视网膜无细胞毛细血管数量增加。在同一批大鼠中,微量营养素可抑制视网膜氧化修饰DNA和硝基酪氨酸的增加以及锰超氧化物歧化酶的减少。糖尿病诱导的线粒体电子传递复合物III(辅酶Q细胞色素c还原酶)和诱导型一氧化氮合酶信使核糖核酸表达的改变也得到了预防。

结论

基于年龄相关性眼病研究的微量营养素通过抑制氧化应激和硝化应激,抑制啮齿动物糖尿病视网膜病变的发展。

临床意义

减缓年龄相关性黄斑变性发病和进展的微量营养素有可能抑制糖尿病视网膜病变的发展。

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