二甲双胍可预防2型糖尿病大鼠肾足细胞损伤。

Experimental Diabetes Research Pub Date : 2012-01-01 Epub Date: 2012-09-27 DOI:10.1155/2012/210821
Junghyun Kim, Eunjin Shon, Chan-Sik Kim, Jin Sook Kim
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引用次数: 105

摘要

高血糖促进氧化应激,从而产生活性氧(ROS),这在糖尿病肾病的发病机制中起着至关重要的作用。二甲双胍是一种口服降糖药,具有抗氧化作用。本文旨在探讨二甲双胍对自发性糖尿病大鼠(SDT)肾足细胞损伤的保护作用。二甲双胍(350 mg/kg/天)给予SDT大鼠17周。检测血糖、糖化血红蛋白(HbA1c)和蛋白尿。检测肾组织病理学、肾8-羟基脱氧鸟苷(8-OHdG)水平及细胞凋亡。43周龄SDT大鼠出现严重高血糖,蛋白尿明显增加。糖尿病引起肾小球结构的显著改变。此外,尿和肾8-OHdG水平高度升高,通过TUNEL和synaptopodin染色显示足细胞丢失。然而,二甲双胍治疗SDT大鼠恢复了所有这些肾脏变化。我们的数据表明,糖尿病肾病中糖尿病引起的足细胞损失可能被抗糖尿病药物二甲双胍通过抑制氧化损伤而抑制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Renal podocyte injury in a rat model of type 2 diabetes is prevented by metformin.

Renal podocyte injury in a rat model of type 2 diabetes is prevented by metformin.

Renal podocyte injury in a rat model of type 2 diabetes is prevented by metformin.

Renal podocyte injury in a rat model of type 2 diabetes is prevented by metformin.

Hyperglycemia promotes oxidative stress and hence generation of reactive oxygen species (ROS), which is known to play a crucial role in the pathogenesis of diabetic nephropathy. Metformin, an oral hypoglycemic drug, possesses antioxidant effects. The aim of this paper is to investigate the protective effects of metformin on the injury of renal podocytes in spontaneously diabetic Torii (SDT) rats, a new model for nonobese type 2 diabetes. Metformin (350 mg/kg/day) was given to SDT rats for 17 weeks. Blood glucose, glycated haemoglobin (HbA1c), and albuminuria were examined. Kidney histopathology, renal 8-hydroxydeoxyguanosine (8-OHdG) levels and apoptosis were examined. In 43-week-old SDT rats, severe hyperglycemia was developed, and albuminuria was markedly increased. Diabetes induced significant alterations in renal glomerular structure. In addition, urinary and renal 8-OHdG levels were highly increased, and podocyte loss was shown through application of the TUNEL and synaptopodin staining. However, treatment of SDT rats with metformin restored all these renal changes. Our data suggested that diabetes-induced podocyte loss in diabetic nephropathy could be suppressed by the antidiabetes drug, metformin, through the repression of oxidative injury.

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来源期刊
Experimental Diabetes Research
Experimental Diabetes Research 医学-内分泌学与代谢
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