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

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 a...

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Autores principales: Kong, Rui, Luo, Hui, Wang, Nan, Li, Jingjing, Xu, Shizan, Chen, Kan, Feng, Jiao, Wu, Liwei, Li, Sainan, Liu, Tong, Lu, Xiya, Xia, Yujing, Shi, Yanhong, Zhou, Yingqun, He, Weigang, Dai, Qi, Zheng, Yuejuan, Lu, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816873/
https://www.ncbi.nlm.nih.gov/pubmed/29483924
http://dx.doi.org/10.1155/2018/6079101
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author Kong, Rui
Luo, Hui
Wang, Nan
Li, Jingjing
Xu, Shizan
Chen, Kan
Feng, Jiao
Wu, Liwei
Li, Sainan
Liu, Tong
Lu, Xiya
Xia, Yujing
Shi, Yanhong
Zhou, Yingqun
He, Weigang
Dai, Qi
Zheng, Yuejuan
Lu, Jie
author_facet Kong, Rui
Luo, Hui
Wang, Nan
Li, Jingjing
Xu, Shizan
Chen, Kan
Feng, Jiao
Wu, Liwei
Li, Sainan
Liu, Tong
Lu, Xiya
Xia, Yujing
Shi, Yanhong
Zhou, Yingqun
He, Weigang
Dai, Qi
Zheng, Yuejuan
Lu, Jie
author_sort Kong, Rui
collection PubMed
description 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.
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spelling pubmed-58168732018-02-26 Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ Kong, Rui Luo, Hui Wang, Nan Li, Jingjing Xu, Shizan Chen, Kan Feng, Jiao Wu, Liwei Li, Sainan Liu, Tong Lu, Xiya Xia, Yujing Shi, Yanhong Zhou, Yingqun He, Weigang Dai, Qi Zheng, Yuejuan Lu, Jie PPAR Res Research Article 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. Hindawi 2018-02-01 /pmc/articles/PMC5816873/ /pubmed/29483924 http://dx.doi.org/10.1155/2018/6079101 Text en Copyright © 2018 Rui Kong et al. https://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Research Article
Kong, Rui
Luo, Hui
Wang, Nan
Li, Jingjing
Xu, Shizan
Chen, Kan
Feng, Jiao
Wu, Liwei
Li, Sainan
Liu, Tong
Lu, Xiya
Xia, Yujing
Shi, Yanhong
Zhou, Yingqun
He, Weigang
Dai, Qi
Zheng, Yuejuan
Lu, Jie
Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title_full Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title_fullStr Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title_full_unstemmed Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title_short Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ
title_sort portulaca extract attenuates development of dextran sulfate sodium induced colitis in mice through activation of pparγ
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816873/
https://www.ncbi.nlm.nih.gov/pubmed/29483924
http://dx.doi.org/10.1155/2018/6079101
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