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Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 9536458, 8 pages
https://doi.org/10.1155/2017/9536458
Research Article

Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

1The First Affiliated Hospital of First Clinical Medical School, Nanjing University of Chinese Medicine, Nanjing 210029, China
2Department of Nephrology, Changshu No. 2 People’s Hospital, Changshu 215500, China
3Department of Second Clinical Medical School, Nanjing University of Chinese Medicine, Nanjing 210029, China

Correspondence should be addressed to Wei Sun; moc.361@iewnussj

Received 31 December 2016; Accepted 27 February 2017; Published 21 March 2017

Academic Editor: Jairo Kennup Bastos

Copyright © 2017 Guang-xing Shui 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

Objectives. The effects of the traditional formula Dahuang Fuzi Decoction (DFD) on chronic aristolochic acid nephropathy (AAN) in mice and its underlying mechanisms were studied. Methods. Mice were randomly divided into the following six groups: the control group, the model group (AAN), the saline-treated group (AAN + vehicle), the normal dose DFD-treated group (AAN + NDFD), the high dose DFD-treated group (AAN + HDFD), and the rosiglitazone treated group (AAN + Rosi). After treating for 8 weeks, 24 h urine and blood samples were collected and the mice sacrificed to study the biochemical parameters associated with renal function. The samples were analyzed for renal fibrosis and mitochondrial dysfunction (MtD) markers. To achieve that, collagen III, collagen I, mitochondrial DNA copy numbers (mtDNA), mitochondrial membrane potential (MMP), ATP content, and ROS production were evaluated. Results. Our results showed that proteinuria, kidney function, and the renal pathological characteristics were improved by DFD and rosiglitazone. The expression of collagen III and collagen I decreased after treating with either DFD or rosiglitazone. Mitochondrial dysfunction based on the increase in ROS production, decrease in mitochondrial DNA copy numbers, and reduction of MMP and ATP content was improved by DFD and rosiglitazone. Conclusions. DFD could protect against renal impairments and ameliorate mitochondrial dysfunction in chronic AAN mice.