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(+)‐Catechin ameliorates diabetic nephropathy by trapping methylglyoxal in type 2 diabetic mice
Author(s) -
Zhu Dina,
Wang Lei,
Zhou Qile,
Yan Shijun,
Li Zhi,
Sheng Jun,
Zhang Wensheng
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400533
Subject(s) - methylglyoxal , glycation , diabetic nephropathy , chemistry , proinflammatory cytokine , endocrinology , advanced glycation end product , nephropathy , medicine , diabetes mellitus , pathogenesis , kidney , oxidative stress , pharmacology , type 2 diabetes , biochemistry , inflammation , enzyme
Scope 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. Methods and results 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 db/db 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. Conclusion 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.