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普洱茶抑制晚期糖基化终产物形成可改善实验性糖尿病肾病的进展。

Inhibition of advanced glycation end product formation by Pu-erh tea ameliorates progression of experimental diabetic nephropathy.

机构信息

State Key Laboratory of Earth Surface Processes and Resource Ecology, Beijing Normal University, Beijing, People's Republic of China.

出版信息

J Agric Food Chem. 2012 Apr 25;60(16):4102-10. doi: 10.1021/jf300347p. Epub 2012 Apr 16.

DOI:10.1021/jf300347p
PMID:22482420
Abstract

Accumulation of advanced glycation end products (AGEs) has been implicated in the development of diabetic nephropathy. We investigated the effects of Pu-erh tea on AGE accumulation associated with diabetic nephropathy. Although it did not affect blood glucose levels and insulin sensitivy, Pu-erh tea treatment for 8 weeks attenuated the increases in urinary albumin, serum creatinine, and mesangial matrix in db/db mice. We found that Pu-erh tea prevented diabetes-induced accumulation of AGEs and led to a decreased level of receptor for AGE expression in glomeruli. Both production and clearance of carbonyl compounds, the main precursor of AGE formation, were probably attenuated by Pu-erh tea in vivo independent of glyoxalase I expression. In vitro, HPLC assay demonstrated Pu-erh tea could trap methylglyoxal in a dose-dependent manner. Our study raises the possibility that inhibition of AGE formation by carbonyl trapping is a promising approach to prevent or arrest the progression of diabetic complications.

摘要

晚期糖基化终产物(AGEs)的积累与糖尿病肾病的发生发展有关。本研究旨在探讨普洱茶对糖尿病肾病相关 AGE 积累的影响。普洱茶处理虽不影响血糖水平和胰岛素敏感性,但可减轻 db/db 小鼠尿白蛋白、血清肌酐和系膜基质的增加,对糖尿病诱导的 AGE 积累具有预防作用,并降低肾小球内 AGE 受体的表达水平。普洱茶可能通过独立于糖氧还蛋白 I 表达来减轻体内羰基化合物(AGE 形成的主要前体)的产生和清除。体外 HPLC 分析表明,普洱茶可剂量依赖性捕获甲基乙二醛。本研究提示,通过羰基捕获抑制 AGE 形成可能是预防或阻止糖尿病并发症进展的一种有前途的方法。

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