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Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 7876064, 12 pages
Research Article

Curcumin Suppresses Intestinal Fibrosis by Inhibition of PPARγ-Mediated Epithelial-Mesenchymal Transition

1First Clinical Medical College, Nanjing University of Chinese Medicine, No. 138 Xianlin Avenue, Nanjing 210023, China
2Department of Colorectal Surgery, The Yancheng Affiliated Hospital of Nanjing University of Chinese Medicine, No. 53 People’s Road, Yancheng 224001, China
3Department of Colorectal Surgery, The Third Affiliated Hospital of Nanjing University of Chinese Medicine, No. 1 Jinling Road, Nanjing 210001, China

Correspondence should be addressed to Li Zeng; moc.361@ilgnibgnez

Received 18 October 2016; Revised 4 December 2016; Accepted 21 December 2016; Published 22 January 2017

Academic Editor: Kuzhuvelil B. Harikumar

Copyright © 2017 Su Xu 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.


Intestinal fibrotic stricture is a major complication of Crohn’s disease (CD) and epithelial-to-mesenchymal transition (EMT) is considered as an important contributor to the formation of intestinal fibrosis by increasing extracellular matrix (ECM) proteins. Curcumin, a compound derived from rhizomes of Curcuma, has been demonstrated with a potent antifibrotic effect. However, its effect on intestinal fibrosis and the potential mechanism is not completely understood. Here we found that curcumin pretreatment significantly represses TGF-β1-induced Smad pathway and decreases its downstream α-smooth muscle actin (α-SMA) gene expression in intestinal epithelial cells (IEC-6); in contrast, curcumin increases expression of E-cadherin and peroxisome proliferator-activated receptor γ (PPARγ) in IEC-6. Moreover, curcumin promotes nuclear translocation of PPARγ and the inhibitory effect of curcumin on EMT could be reversed by PPARγ antagonist GW9662. Consistently, in the rat model of intestinal fibrosis induced by 2,4,5-trinitrobenzene sulphonic acid (TNBS), oral curcumin attenuates intestinal fibrosis by increasing the expression of PPARγ and E-cadherin and decreasing the expression of α-SMA, FN, and CTGF in colon tissue. Collectively, these results indicated that curcumin is able to prevent EMT progress in intestinal fibrosis by PPARγ-mediated repression of TGF-β1/Smad pathway.