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GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model

Ulcerative colitis (UC) is an inflammatory bowel disease. The intake of African Garcinia Kola nuts has been reported as a therapy for diarrhea and dysentery in the African population. However, the mechanism of action through which Garcinia Kola nuts act to ameliorates UC remains unknown. GB1a is the...

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Autores principales: Yu, Yuanyuan, Zheng, Congmin, Lu, Xu, Deng, Changsheng, Xu, Qin, Guo, Wenfeng, Wu, Qingye, Wang, Qi, Liu, Changhui, Huang, Xinan, Song, Jianping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8452853/
https://www.ncbi.nlm.nih.gov/pubmed/34557497
http://dx.doi.org/10.3389/fmed.2021.654867
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author Yu, Yuanyuan
Zheng, Congmin
Lu, Xu
Deng, Changsheng
Xu, Qin
Guo, Wenfeng
Wu, Qingye
Wang, Qi
Liu, Changhui
Huang, Xinan
Song, Jianping
author_facet Yu, Yuanyuan
Zheng, Congmin
Lu, Xu
Deng, Changsheng
Xu, Qin
Guo, Wenfeng
Wu, Qingye
Wang, Qi
Liu, Changhui
Huang, Xinan
Song, Jianping
author_sort Yu, Yuanyuan
collection PubMed
description Ulcerative colitis (UC) is an inflammatory bowel disease. The intake of African Garcinia Kola nuts has been reported as a therapy for diarrhea and dysentery in the African population. However, the mechanism of action through which Garcinia Kola nuts act to ameliorates UC remains unknown. GB1a is the main active component of Garcinia Kola nuts. In this study, we explored the therapeutic effects and underlying mechanism of GB1a on dextran sodium sulfate (DSS)-induced UC. Human Colonic Epithelial Cells (HCoEpic) were challenged with TNF-α to test the effects of GB1a in protecting against oxidative stress and inflammation in vitro. Our data showed that GB1a significantly attenuated DSS-induced colonic inflammatory injury manifested as reversed loss of body weight and disease activity index (DAI) scores in UC mice. We also showed that GB1a improved the permeability of the intestinal epithelium by modulating the expression of tight junction proteins (ZO-1, Occludin). Mechanistically, GB1a may activate the Nrf2 antioxidant signaling pathway and suppress the nuclear translocation of NF-κB in reduced oxidative stress and expression of inflammatory genes induced by TNF-α in HCoEpic cells. Our study suggests that GB1a alleviates inflammation, oxidative stress and the permeability of the colonic epithelial mucosa in UC mice via the repression of NF-κB and activation of Nrf2 signaling pathway.
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spelling pubmed-84528532021-09-22 GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model Yu, Yuanyuan Zheng, Congmin Lu, Xu Deng, Changsheng Xu, Qin Guo, Wenfeng Wu, Qingye Wang, Qi Liu, Changhui Huang, Xinan Song, Jianping Front Med (Lausanne) Medicine Ulcerative colitis (UC) is an inflammatory bowel disease. The intake of African Garcinia Kola nuts has been reported as a therapy for diarrhea and dysentery in the African population. However, the mechanism of action through which Garcinia Kola nuts act to ameliorates UC remains unknown. GB1a is the main active component of Garcinia Kola nuts. In this study, we explored the therapeutic effects and underlying mechanism of GB1a on dextran sodium sulfate (DSS)-induced UC. Human Colonic Epithelial Cells (HCoEpic) were challenged with TNF-α to test the effects of GB1a in protecting against oxidative stress and inflammation in vitro. Our data showed that GB1a significantly attenuated DSS-induced colonic inflammatory injury manifested as reversed loss of body weight and disease activity index (DAI) scores in UC mice. We also showed that GB1a improved the permeability of the intestinal epithelium by modulating the expression of tight junction proteins (ZO-1, Occludin). Mechanistically, GB1a may activate the Nrf2 antioxidant signaling pathway and suppress the nuclear translocation of NF-κB in reduced oxidative stress and expression of inflammatory genes induced by TNF-α in HCoEpic cells. Our study suggests that GB1a alleviates inflammation, oxidative stress and the permeability of the colonic epithelial mucosa in UC mice via the repression of NF-κB and activation of Nrf2 signaling pathway. Frontiers Media S.A. 2021-09-07 /pmc/articles/PMC8452853/ /pubmed/34557497 http://dx.doi.org/10.3389/fmed.2021.654867 Text en Copyright © 2021 Yu, Zheng, Lu, Deng, Xu, Guo, Wu, Wang, Liu, Huang and Song. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Medicine
Yu, Yuanyuan
Zheng, Congmin
Lu, Xu
Deng, Changsheng
Xu, Qin
Guo, Wenfeng
Wu, Qingye
Wang, Qi
Liu, Changhui
Huang, Xinan
Song, Jianping
GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title_full GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title_fullStr GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title_full_unstemmed GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title_short GB1a Ameliorates Ulcerative Colitis via Regulation of the NF-κB and Nrf2 Signaling Pathways in an Experimental Model
title_sort gb1a ameliorates ulcerative colitis via regulation of the nf-κb and nrf2 signaling pathways in an experimental model
topic Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8452853/
https://www.ncbi.nlm.nih.gov/pubmed/34557497
http://dx.doi.org/10.3389/fmed.2021.654867
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