Shi-Jun Yan^†,‡,§, Lei Wang^†,‡,§, Zhi Li^†,‡,§, Di-Na Zhu^†,‡,§, Shao-Chen Guo^†,‡,§, Wen-Feng Xin^†,‡,§, Yan-Fang Yang^†, Xiao Cong^†,‡,§, Tao Ma^∥, Pei-Ping Shen^#, Jun Sheng^⊥,#, Wen-Sheng Zhang^†,‡,§,#

^†State Key Laboratory of Earth Surface Processes and Resource Ecology, Beijing Normal University, Beijing 100088, People’s Republic of China;

^‡Beijing Area Major Laboratory of Protection and Utilization of Traditional Chinese Medicine, Beijing 100875, People’s Republic of China;

^§Center for Natural Medicine Engineering, Ministry of Education of the People’s Republic of China, Beijing 100088, People’s Republic of China;

^∥Dongfang Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100078, People’s Republic of China;

^⊥Molecular Biology Laboratory, Yunnan Agricultural University, Northern Suburb of Kunming, Yunnan Province 650201, People’s Republic of China;

^#Beijing Pu’er Tea Research Institute, Beijing 100875, People’s Republic of China.

 

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.

 

Keywords: Pu-erh tea, rosiglitazone, diabetic nephropathy, db/db mice, methylglyoxal, advanced glycation end products, RAGE, glyoxalase I