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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 367040, 9 pages
Research Article

Magnolia Extract (BL153) Ameliorates Kidney Damage in a High Fat Diet-Induced Obesity Mouse Model

1The Second Hospital of Jilin University, Changchun 130041, China
2The Kosair Children’s Hospital Research Institute, Department of Pediatrics of the University of Louisville, Louisville, KY 20202, USA
3School of Public Health, Jilin University, Changchun 130021, China
4The First Hospital of Jilin University, Changchun 130021, China
5Bioland Biotec Co., Ltd., Zhangjiang Modern Medical Device Park, Pudong, Shanghai 201201, China
6Bioland R&D Center, 59 Songjeongni 2-gil, Byeongcheon, Dongnam, Cheonan, Chungnam 330-863, Republic of Korea

Received 19 September 2013; Revised 31 October 2013; Accepted 6 November 2013

Academic Editor: Joseph Fomusi Ndisang

Copyright © 2013 Wenpeng Cui 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.


Accumulating evidence demonstrated that obesity is a risk factor for renal structural and functional changes, leading to the end-stage renal disease which imposes a heavy economic burden on the community. However, no effective therapeutic method for obesity-associated kidney disease is available. In the present study, we explored the therapeutic potential of a magnolia extract (BL153) for treating obesity-associated kidney damage in a high fat diet- (HFD-) induced mouse model. The results showed that inflammation markers (tumor necrosis factor-α and plasminogen activator inhibitor-1) and oxidative stress markers (3-nitrotyrosine and 4-hydroxy-2-nonenal) were all significantly increased in the kidney of HFD-fed mice compared to mice fed with a low fat diet (LFD). Additionally, proteinuria and renal structure changes in HFD-fed mice were much more severe than that in LFD-fed mice. However, all these alterations were attenuated by BL153 treatment, accompanied by upregulation of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and hexokinase II (HK II) expression in the kidney. The present study indicates that BL153 administration may be a novel approach for renoprotection in obese individuals by antiinflammation and anti-oxidative stress most likely via upregulation of PGC-1α and HK II signal in the kidney.