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Evidence-Based Complementary and Alternative Medicine
Volume 2015 (2015), Article ID 827472, 12 pages
http://dx.doi.org/10.1155/2015/827472
Research Article

The Protective Effects of Curcumin on Obesity-Related Glomerulopathy Are Associated with Inhibition of Wnt/β-Catenin Signaling Activation in Podocytes

1Division of Nephrology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China
2Division of Nephrology, Beijing Traditional Chinese Medicine Hospital, Capital Medical University, Beijing 100010, China

Received 3 February 2015; Accepted 14 March 2015

Academic Editor: Dan Hu

Copyright © 2015 Bao-li Liu 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.

Abstract

The present study investigated the effects of curcumin, one of the most important active ingredients of turmeric, on podocyte injury in vitro and obesity-related glomerulopathy (ORG) in vivo. Cellular experiments in vitro showed that curcumin significantly antagonized leptin-induced downregulation of the mRNA and protein expression of podocyte-associated molecules including nephrin, podocin, podoplanin, and podocalyxin. Animal experiments in vivo showed that curcumin significantly reduced the body weight, Lee’s index, abdominal fat index, urinary protein excretion, and average glomerular diameter and significantly upregulated the mRNA and protein expressions of the above podocyte-associated molecules in ORG mice. Furthermore, the experiments in vitro and in vivo both displayed that curcumin could downregulate the mRNA and protein expressions of Wnt1, Wnt2b, Wnt6, and β-catenin and upregulate the phosphorylation level of β-catenin protein in podocytes and renal tissue. In conclusion, curcumin is able to alleviate the harmful reaction of leptin on podocytes and reduce the severity of ORG. The above protective effects are associated with the inhibition of Wnt/β-catenin signaling activation in podocytes.