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PPAR Research
Volume 2018, Article ID 6079101, 11 pages
https://doi.org/10.1155/2018/6079101
Research Article

Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ

1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China
2The School of Medicine, Soochow University, Suzhou 215006, China
3Department of Gastroenterology, Shanghai Tenth Hospital, School of Clinical Medicine, Nanjing Medical University, Shanghai 200072, China
4Department of Immunology and Microbiology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
5The Eye Hospital, Wenzhou Medical University, Wenzhou City, Zhejiang 325027, China

Correspondence should be addressed to Qi Dai; nc.ca.eye.liam@qd, Yuejuan Zheng; moc.361@21467714631, and Jie Lu; moc.liamtoh@nersinnek

Received 27 July 2017; Revised 14 September 2017; Accepted 28 November 2017; Published 1 February 2018

Academic Editor: Yuewen Gong

Copyright © 2018 Rui Kong 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

Portulaca oleracea L. is a traditional Chinese medicine, which has been used as adjuvant therapy for inflammatory bowel disease (IBD). However, the mechanism of its activity in IBD still remains unclear. Since previous studies have documented the anti-inflammatory effect of peroxisome proliferator activated receptors-γ (PPAR-γ), Portulaca regulation of PPAR-γ in inflammation was examined in current study. Ulcerative colitis (UC) was generated by 5% dextran sulfate sodium (DSS) in mice and four groups were established as normal control, DSS alone, DSS plus mesalamine, and DSS plus Portulaca. Severity of UC was evaluated by body weight, stool blood form, and length of colorectum. Inflammation was examined by determination of inflammatory cytokines (TNF-a, IL-6, and IL-1a). Portulaca extract was able to attenuate development of UC in DSS model similar to the treatment of mesalazine. Moreover, Portulaca extract inhibited proinflammatory cytokines release and reduced the level of DSS-induced NF-κB phosphorylation. Furthermore, Portulaca extract restored PPAR-γ level, which was reduced by DSS. In addition, Portulaca extract protected DSS induced apoptosis in mice. In conclusion, Portulaca extract can alleviate colitis in mice through regulation of inflammatory reaction, apoptosis, and PPAR-γ level; therefore, Portulaca extract can be a potential candidate for the treatment of IBD.