(+)‐Catechin ameliorates diabetic nephropathy by trapping methylglyoxal in type 2 diabetic mice. Issue 12 (27th October 2014)

• Record Type: Journal Article
• Authors: Zhu, Dina; Wang, Lei; Zhou, Qile; Yan, Shijun; Li, Zhi; Sheng, Jun; Zhang, Wensheng
• Is Part Of: Molecular nutrition & food research. Volume 58:Issue 12(2014:Dec.)
• Page Start: 2249
• Page End: 2260
• Publication Date: 2014-10-27
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201400533
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2271-sec-0010" sec-type="section"> <title>Scope</title> <p>Accumulation of glycolytic metabolite methylglyoxal (MG) in diabetic kidney is thought to contribute to the pathogenesis of nephropathy, either as a direct toxin or as a precursor for advanced glycation end products (AGEs). Using (+)‐catechin (CE), a novel MG trapper, we investigated whether MG trapping is sufficient to prevent the progression of diabetic nephropathy in type 2 diabetic mice.</p> </sec> <sec id="mnfr2271-sec-0020" sec-type="section"> <title>Methods and results</title> <p>CE markedly trapped exogenous MG in a time‐ and dose‐dependent manner and formed mono‐MG‐CE and di‐MG‐CE adducts, which were characterized by HPLC‐ESI‐Q‐TOFMS. In vivo, CE administration for 16 wk significantly ameliorated renal dysfunction in type 2 diabetic <italic>db/db</italic> mice, partially due to MG trapping, which in turn inhibited AGEs formation and lowered proinflammatory cytokines, including tumor necrosis factor α and IL‐1β. Similarly, the MG trapping and cellular signaling inhibition effects of CE were observed in human endothelium‐derived cells under high glucose conditions.</p> </sec> <sec id="mnfr2271-sec-0030" sec-type="section"> <title>Conclusion</title> <p>CE might ameliorate renal dysfunction in diabetic mice as consequences of inhibiting AGEs formation and cutting off inflammatory pathway via MG trapping. Thus, CE may be a potential natural product as an MG scavenger against diabetes‐related complications.</p> </sec> </abstract>