Renal Podocyte Apoptosis in Zucker Diabetic Fatty Rats: Involvement of Methylglyoxal-Induced Oxidative DNA Damage

被引：18

作者：

Kim, J. ^{[1
]}

Sohn, E. ^{[1
]}

Kim, C. -S. ^{[1
]}

Kim, J. S. ^{[1
]}

机构：

[1] Korea Inst Oriental Med, Diabet Complicat Res Ctr, Div Tradit Korean Med TKM Integrated Res, Taejon, South Korea

来源：

JOURNAL OF COMPARATIVE PATHOLOGY | 2011年 / 144卷 / 01期

关键词：

apoptosis; diabetic nephropathy; methylglyoxal; oxidative stress; podocyte; ADVANCED GLYCATION; NEPHROPATHY; ACTIVATION; GLYOXAL; STRESS; PATHOGENESIS; PROTEINURIA; PROTECTS; SYSTEM; KINASE;

D O I：

10.1016/j.jcpa.2010.04.008

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

Methylglyoxal (MGO) is a cytotoxic metabolite produced by in-vivo glycolysis that may result in diabetic complications. The aim of this study was to determine whether MGO and oxidative stress caused apoptosis of renal podocytes in the Zucker diabetic fatty (ZDF) rat, an animal model of type 2 diabetes mellitus. Male ZDF rats aged 21 weeks developed marked hyperglycaemia with proteinuria and albuminuria. Immunohistochemical evaluation of sections of kidney demonstrated expression of MGO and 8-hydroxydeoxyguanosine (8-OHdG) in the podocytcs of both normoglycaemic and diabetic rats. Podocyte apoptosis was shown through application of the TUNEL method. These findings suggest that expression of MGO and 8-OHdG is caused by hyperglycaemia, and that this expression is associated with the observed apoptosis of podocytes and is related to diabetic nephropathy. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：41 / 47

页数：7

共 40 条

[1] Glyoxal and methylglyoxal trigger distinct signals for map family kinases and caspase activation in human endothelial cells [J].