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 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.