Nicousamide blocks the effects of advanced glycation end products on renal cells

被引：11

作者：

Li, Hongyan ^{[1
,2
,3
]}

Zhang, Yi ^{[1
,2
]}

Wang, Hongbo ^{[1
,2
]}

Zheng, Xuguang ^{[1
,2
]}

Chen, Xiaoguang ^{[1
,2
]}

机构：

[1] Chinese Acad Med Sci, Dept Pharmacol, Inst Mat Med, Beijing 100050, Peoples R China

[2] Peking Union Med Coll, Beijing 100050, Peoples R China

[3] NIDDK, NIH, Bethesda, MD USA

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2012年 / 674卷 / 2-3期

基金：

中国国家自然科学基金;

关键词：

Nicousamide; AGE (Advanced glycation end products); TGF-beta 1 (Transforming growth factor-beta 1); CTGF (Connective tissue growth factor); MMPs (Matrix metalloproteinase); TISSUE GROWTH-FACTOR; RAT MESANGIAL CELLS; DIABETIC-NEPHROPATHY; EXTRACELLULAR-MATRIX; MAILLARD REACTION; FACTOR-BETA; IN-VITRO; COMPLICATIONS; PROGRESSION; EXPRESSION;

D O I：

10.1016/j.ejphar.2011.06.056

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Advanced glycation end products (AGE) are key factors in the pathogenesis of diabetic nephropathy. AGE can stimulate the expressions of fibrogenic transforming growth factor (TGF-beta 1) and connective tissue growth factor (CTGF), which in turn induce renal hypertrophy, sclerosis and functional failure. The purpose of this study was to examine nicousamide, a novel coumarin aspirin derivative, in the treatment of diabetic nephropathy using a renal mesangial and tubular epithelia cell model. RT-PCR and ELISA analyses showed that nicousamide inhibited AGE-induced TGF-beta 1 and CTGF. Nicousamide blocked AGE-induced G1-arrest in mesangial cells and tubular epithelia by flow cytometry. Suppression of matrix metalloproteinase activity by AGE was restored by nicousamide. This study supports that nicousamide retards diabetic nephropathy by blocking the effects of AGE on renal cells. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：455 / 459

页数：5

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