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Journal of Diabetes Research
Volume 2016 (2016), Article ID 8738760, 13 pages
http://dx.doi.org/10.1155/2016/8738760
Research Article

Naringenin Ameliorated Kidney Injury through Let-7a/TGFBR1 Signaling in Diabetic Nephropathy

1Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China
2Department of Cell Biology and Genetics, Chongqing Medical University, Chongqing 400016, China
3Department of Bioinformatics, Chongqing Medical University, Chongqing 400016, China
4Chongqing Red Cross Hospital, Chongqing 400016, China
5The Second Clinical College, Chongqing Medical University, Chongqing 400016, China
6The First Clinical College, Chongqing Medical University, Chongqing 400016, China

Received 1 April 2016; Revised 25 May 2016; Accepted 1 June 2016

Academic Editor: Mark A. Yorek

Copyright © 2016 Ning Yan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus (DM). However, the exact mechanism is not clearly understood. In this study, our results showed that 24 h urinary protein, kidney index, and glomerular area were decreased, while creatinine clearance ratio was increased in DN rats when the rats were treated with NAR 50 mg/d for 6 weeks. Mesangial cell (MMCs) proliferation was inhibited in the NAR group by 3,(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), and the cell cycle analysis showed that cells stayed in G2 phase in NAR group. And NAR treatment attenuated the deposition of ECM in DN rats and MMCs. Moreover, our data showed that let-7a was downexpressed in both DN rats and MMCs under high glucose condition. Surprisingly, NAR affected the expressions of Col4 and FN through upregulating let-7a in MMCs. In addition, we found that let-7a negatively regulated the expression of transforming growth factor-β1 receptor 1 (TGFBR1), and TGFBR1 was required for the let-7a-mediated downregulation of TGF-β1/smad signaling. Interestingly, NAR inhibited TGF-β1/smads signaling activation by upregulating let-7a. Therefore, our findings indicated that NAR ameliorated kidney injury by regulating let-7a/TGFBR1 signaling.