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首页> 外文期刊>Bioorganic and Medicinal Chemistry Letters >The effects of aminoguanidine on retinopathy in STZ-induced diabetic rats
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The effects of aminoguanidine on retinopathy in STZ-induced diabetic rats

机译：氨基胍对STZ诱导糖尿病大鼠视网膜病变的影响

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Background: The accumulation of advanced glycated end products (AGEs) in retinal blood vessels is one of the major etiological factors contributing to diabetic retinopathy. Aminoguanidine (AG) is one of the most extensively used inhibitors of AGEs formation. The aim of this study was to investigate whether AG could protect the development of diabetic retinopathy through inhibition of AGEs. Methods: Rat diabetes was induced by intraperitoneal injection with streptozotocin (STZ). AG was given to rats in drinking water. Retina was extracted 3 and 6 months following STZ and AG administration. Immunochemistry and transmission electron microscope were used to detect the expression of AGEs and retina morphology. Results: Extensive staining of AGEs was detected in retinal blood vessels of 3- and 6-month diabetic rats, while no significant staining was found in the control non-diabetic retina or AG treated groups. Pericyte loss, endothelial cell proliferation, increased ratio of endothelial cells/pericytes, acellular capillaries and capillary occlusion were observed in the retina of 6-month diabetic rats. The increased electron density of retinal capillary basement membrane, mitochondrial swelling in pericytes and endothelial cells were also found in 6-month diabetic rats. The 3-month diabetic rats and the AG-treated rats did not have similar morphological changes compared to control group. The AGEs staining in AG-treated rats was still weakly positive. Conclusions: AGEs plays pivotal roles in diabetic retinopathy. AGE deposition occurs prior to retinal microvasculature changes. AG could prevent the onset and development of diabetic retinopathy through inhibition of AGEs.
机译：背景：视网膜血管中晚期糖化末端产品（年龄）的积累是患糖尿病视网膜病变的主要病因因素之一。氨基胍（AG）是最广泛使用的年龄形成的抑制剂之一。本研究的目的是通过抑制年龄来研究AG是否可以保护糖尿病视网膜病变的发展。方法：通过腹膜内注射用链脲佐菌素（STZ）诱导大鼠糖尿病。 AG给饮用水中的大鼠。在STZ和Ag给药后3和6个月提取视网膜。免疫化学和透射电子显微镜用于检测年龄和视网膜形态的表达。结果：在3个月和6个月糖尿病大鼠的视网膜血管中检测到大量染色，而控制非糖尿病视网膜或AG处理基团没有明显的染色。在6个月的糖尿病大鼠的视网膜中观察到细胞损失，内皮细胞增殖，内皮细胞/周细胞，细胞毛细血管和毛细血管闭塞的增加。在6个月的糖尿病大鼠中还发现了视网膜毛细管基底膜的电子密度，眼镜细胞和内皮细胞的线粒体肿胀。与对照组相比，3个月的糖尿病大鼠和Ag治疗的大鼠没有相似的形态变化。 Ag治疗大鼠染色的年龄仍然弱呈阳性。结论：年龄在糖尿病视网膜病变中发挥枢轴作用。在视网膜微血管结构发生之前发生年龄沉积。 AG可以通过抑制年龄来防止糖尿病视网膜病变的发病和发展。

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