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

Author:

Cui Wenpeng12,Wang Yangwei12,Chen Qiang23,Sun Weixia24,Cai Lu2,Tan Yi2,Kim Ki-Soo5,Kim Ki Ho6,Kim Young Heui6

Affiliation:

1. The Second Hospital of Jilin University, Changchun 130041, China

2. The Kosair Children’s Hospital Research Institute, Department of Pediatrics of the University of Louisville, Louisville, KY 20202, USA

3. School of Public Health, Jilin University, Changchun 130021, China

4. The First Hospital of Jilin University, Changchun 130021, China

5. Bioland Biotec Co., Ltd., Zhangjiang Modern Medical Device Park, Pudong, Shanghai 201201, China

6. Bioland R&D Center, 59 Songjeongni 2-gil, Byeongcheon, Dongnam, Cheonan, Chungnam 330-863, Republic of Korea

Abstract

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 amagnoliaextract (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-αand 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-γcoactivator-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-1αand HK II signal in the kidney.

Funder

Chungbuk Technopark Grant Bio-International Collaborating Research

Publisher

Hindawi Limited

Subject

Cell Biology,Ageing,General Medicine,Biochemistry

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