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MagnoliaExtract (BL153) Ameliorates Kidney Damage in a High Fat Diet-Induced Obesity Mouse Model
Author(s) -
Wenpeng Cui,
Yangwei Wang,
Qiang Chen,
Weixia Sun,
Lu Cai,
Yi Tan,
Ki-Soo Kim,
Ki Ho Kim,
Young Heui Kim
Publication year - 2013
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2013/367040
Subject(s) - endocrinology , medicine , oxidative stress , kidney , kidney disease , nitrotyrosine , downregulation and upregulation , inflammation , peroxisome proliferator activated receptor , plasminogen activator inhibitor 1 , plasminogen activator , biology , receptor , nitric oxide , biochemistry , nitric oxide synthase , gene
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-1 α (PGC-1 α ) 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-1 α and HK II signal in the kidney.

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