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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 7496930, 10 pages
Research Article

MnTBAP Therapy Attenuates Renal Fibrosis in Mice with 5/6 Nephrectomy

Jing Yu,1,2,3 Song Mao,1,2,3 Yue Zhang,1,2,3 Wei Gong,1,3 Zhanjun Jia,1,2,3 Songming Huang,1,2,3 and Aihua Zhang1,2,3

1Department of Nephrology, Nanjing Children’s Hospital, Nanjing Medical University, Nanjing 210008, China
2Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing 210029, China
3Nanjing Key Laboratory of Pediatrics, Nanjing 210008, China

Received 1 December 2015; Accepted 20 January 2016

Academic Editor: Alexandra Scholze

Copyright © 2016 Jing Yu 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.


Renal fibrosis is a common pathological feature of all kinds of chronic kidney diseases (CKDs) with uncertain mechanisms. Accumulating evidence demonstrated an important role of oxidative stress in the pathogenesis of CKD. Here we hypothesized that MnTBAP (manganese (III) tetrakis (4-benzoic acid)porphyrin chloride), a cell-permeable mimic of superoxide dismutase (SOD), may protect against the fibrotic response in CKD by antagonizing oxidative stress. To verify this hypothesis, we performed experiments in tubular epithelial cells and mice with 5/6 nephrectomy (Nx). In mouse tubular epithelial cells, TGF-β1 induced a significant transition to fibrotic phenotype in line with a remarkable mitochondrial dysfunction, which was markedly improved by MnTBAP (1.14 μM) pretreatment. In remnant kidneys of 5/6 Nx mice, tubulointerstitial fibrosis occurred in parallel with mitochondrial abnormality in renal tubular cells. Administration of MnTBAP significantly attenuated the deposition of extracellular matrix as evidenced by the blocked expressions of fibronectin, collagen I, and collagen III. Masson staining also displayed an ameliorated accumulation of collagenous matrix in MnTBAP-treated mice. Moreover, MnTBAP also significantly improved the severity of proteinuria without altering CKD-related hypertension. Collectively, MnTBAP therapy served as a promising strategy in preventing renal fibrosis in CKDs possibly via antagonizing mitochondrial-derived oxidative stress and subsequent protection of mitochondrial function.