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Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway
Ulcerative colitis (UC) is a refractory chronic disease characterized by bloody diarrhea and mucosal or submucosal ulcers. There is an urgent need of new drugs for the treatment of ulcerative colitis. EHLJ7 is a quaternary coptisine derivative. Herein, we explored the therapeutic effect of EHLJ7 on...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6987075/ https://www.ncbi.nlm.nih.gov/pubmed/32038241 http://dx.doi.org/10.3389/fphar.2019.01553 |
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author | Tang, Xiaonan Li, Xiang Wang, Yufei Zhang, ZhiHui Deng, AnJun Wang, WenJie Zhang, Haijing Qin, Hailin Wu, LianQiu |
author_facet | Tang, Xiaonan Li, Xiang Wang, Yufei Zhang, ZhiHui Deng, AnJun Wang, WenJie Zhang, Haijing Qin, Hailin Wu, LianQiu |
author_sort | Tang, Xiaonan |
collection | PubMed |
description | Ulcerative colitis (UC) is a refractory chronic disease characterized by bloody diarrhea and mucosal or submucosal ulcers. There is an urgent need of new drugs for the treatment of ulcerative colitis. EHLJ7 is a quaternary coptisine derivative. Herein, we explored the therapeutic effect of EHLJ7 on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice. Results showed that EHLJ7 have good effects on DSS-induced colitis. EHLJ7 significantly improved symptoms induced by DSS including of weight loss, colon contracture, disease activity index (DAI), inflammatory infiltration, and so on. Furthermore, results showed that EHLJ7 could enhance short-chain fatty acids (SCFAs) production especially butyric acid, suggesting that EHLJ7 could improve the metabolic disorder of intestinal flora to a certain extent. Further study indicated that EHLJ7 could cooperate with butyrate to exert its anti-ulcerative colitis effect by inhibiting the activation of janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 1 (SOCS1) pathway. Therefore, EHLJ7 has a potential to be developed as a candidate for the treatment of colitis. |
format | Online Article Text |
id | pubmed-6987075 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-69870752020-02-07 Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway Tang, Xiaonan Li, Xiang Wang, Yufei Zhang, ZhiHui Deng, AnJun Wang, WenJie Zhang, Haijing Qin, Hailin Wu, LianQiu Front Pharmacol Pharmacology Ulcerative colitis (UC) is a refractory chronic disease characterized by bloody diarrhea and mucosal or submucosal ulcers. There is an urgent need of new drugs for the treatment of ulcerative colitis. EHLJ7 is a quaternary coptisine derivative. Herein, we explored the therapeutic effect of EHLJ7 on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice. Results showed that EHLJ7 have good effects on DSS-induced colitis. EHLJ7 significantly improved symptoms induced by DSS including of weight loss, colon contracture, disease activity index (DAI), inflammatory infiltration, and so on. Furthermore, results showed that EHLJ7 could enhance short-chain fatty acids (SCFAs) production especially butyric acid, suggesting that EHLJ7 could improve the metabolic disorder of intestinal flora to a certain extent. Further study indicated that EHLJ7 could cooperate with butyrate to exert its anti-ulcerative colitis effect by inhibiting the activation of janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 1 (SOCS1) pathway. Therefore, EHLJ7 has a potential to be developed as a candidate for the treatment of colitis. Frontiers Media S.A. 2020-01-22 /pmc/articles/PMC6987075/ /pubmed/32038241 http://dx.doi.org/10.3389/fphar.2019.01553 Text en Copyright © 2020 Tang, Li, Wang, Zhang, Deng, Wang, Zhang, Qin and Wu http://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 | Pharmacology Tang, Xiaonan Li, Xiang Wang, Yufei Zhang, ZhiHui Deng, AnJun Wang, WenJie Zhang, Haijing Qin, Hailin Wu, LianQiu Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title | Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title_full | Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title_fullStr | Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title_full_unstemmed | Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title_short | Butyric Acid Increases the Therapeutic Effect of EHLJ7 on Ulcerative Colitis by Inhibiting JAK2/STAT3/SOCS1 Signaling Pathway |
title_sort | butyric acid increases the therapeutic effect of ehlj7 on ulcerative colitis by inhibiting jak2/stat3/socs1 signaling pathway |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6987075/ https://www.ncbi.nlm.nih.gov/pubmed/32038241 http://dx.doi.org/10.3389/fphar.2019.01553 |
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