Indole-3-acetic acid ameliorates dextran sulfate sodium-induced colitis via the ERK signaling pathway

IF 6.9 3区 医学 Q1 CHEMISTRY, MEDICINAL Archives of Pharmacal Research Pub Date : 2024-03-15 DOI:10.1007/s12272-024-01488-z
Xinyan Qu, Yingying Song, Qingjun Li, Qi Xu, Yanru Li, Huimin Zhang, Xuemei Cheng, Charles R. Mackay, Quanbo Wang, Wei Liu
{"title":"Indole-3-acetic acid ameliorates dextran sulfate sodium-induced colitis via the ERK signaling pathway","authors":"Xinyan Qu,&nbsp;Yingying Song,&nbsp;Qingjun Li,&nbsp;Qi Xu,&nbsp;Yanru Li,&nbsp;Huimin Zhang,&nbsp;Xuemei Cheng,&nbsp;Charles R. Mackay,&nbsp;Quanbo Wang,&nbsp;Wei Liu","doi":"10.1007/s12272-024-01488-z","DOIUrl":null,"url":null,"abstract":"<div><p>Microbiota-derived catabolism of nutrients is closely related to ulcerative colitis (UC). The level of indole-3-acetic acid (IAA), a microbiota-dependent metabolite of tryptophan, was decreased significantly in the feces of UC patients. Thus supplementation with IAA could be a potential therapeutic method for ameliorating colitis. In this work, the protective effect of supplementation with IAA on dextran sulfate sodium (DSS)-induced colitis was evaluated, and the underlying mechanism was elucidated. The results indicated that the administration of IAA significantly relieved DSS-induced weight loss, reduced the disease activity index (DAI), restored colon length, alleviated intestinal injury, and improved the intestinal tight junction barrier. Furthermore, IAA inhibited intestinal inflammation by reducing the expression of proinflammatory cytokines and promoting the production of IL-10 and TGF-β1. In addition, the ERK signaling pathway is an important mediator of various physiological processes including inflammatory responses and is closely associated with the expression of IL-10. Notably, IAA treatment induced the activation of extracellular signal-regulated kinase (ERK), which is involved in the progression of colitis, while the ERK inhibitor U0126 attenuated the beneficial effects of IAA. In summary, IAA could attenuate the clinical symptoms of colitis, and the ERK signaling pathway was involved in the underlying mechanism. Supplementation with IAA could be a potential option for preventing or ameliorating UC.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 3","pages":"288 - 299"},"PeriodicalIF":6.9000,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Pharmacal Research","FirstCategoryId":"3","ListUrlMain":"https://link.springer.com/article/10.1007/s12272-024-01488-z","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
引用次数: 0

Abstract

Microbiota-derived catabolism of nutrients is closely related to ulcerative colitis (UC). The level of indole-3-acetic acid (IAA), a microbiota-dependent metabolite of tryptophan, was decreased significantly in the feces of UC patients. Thus supplementation with IAA could be a potential therapeutic method for ameliorating colitis. In this work, the protective effect of supplementation with IAA on dextran sulfate sodium (DSS)-induced colitis was evaluated, and the underlying mechanism was elucidated. The results indicated that the administration of IAA significantly relieved DSS-induced weight loss, reduced the disease activity index (DAI), restored colon length, alleviated intestinal injury, and improved the intestinal tight junction barrier. Furthermore, IAA inhibited intestinal inflammation by reducing the expression of proinflammatory cytokines and promoting the production of IL-10 and TGF-β1. In addition, the ERK signaling pathway is an important mediator of various physiological processes including inflammatory responses and is closely associated with the expression of IL-10. Notably, IAA treatment induced the activation of extracellular signal-regulated kinase (ERK), which is involved in the progression of colitis, while the ERK inhibitor U0126 attenuated the beneficial effects of IAA. In summary, IAA could attenuate the clinical symptoms of colitis, and the ERK signaling pathway was involved in the underlying mechanism. Supplementation with IAA could be a potential option for preventing or ameliorating UC.

Abstract Image

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
吲哚-3-乙酸通过 ERK 信号通路改善右旋糖酐硫酸钠诱导的结肠炎。
微生物群衍生的营养物质分解与溃疡性结肠炎(UC)密切相关。吲哚-3-乙酸(IAA)是色氨酸的一种依赖微生物群的代谢产物,在溃疡性结肠炎患者粪便中的含量明显下降。因此,补充 IAA 可能是改善结肠炎的一种潜在治疗方法。本研究评估了补充IAA对葡聚糖硫酸钠(DSS)诱导的结肠炎的保护作用,并阐明了其潜在机制。结果表明,服用IAA能明显缓解右旋糖酐硫酸钠诱导的体重下降,降低疾病活动指数(DAI),恢复结肠长度,减轻肠道损伤,改善肠道紧密连接屏障。此外,IAA 还能减少促炎细胞因子的表达,促进 IL-10 和 TGF-β1 的产生,从而抑制肠道炎症。此外,ERK 信号通路是包括炎症反应在内的各种生理过程的重要介质,与 IL-10 的表达密切相关。值得注意的是,IAA处理会诱导细胞外信号调节激酶(ERK)的活化,而ERK抑制剂U0126会减弱IAA的有益作用。综上所述,IAA能减轻结肠炎的临床症状,而ERK信号通路参与了其潜在机制。补充IAA可能是预防或改善UC的一种潜在选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
13.40
自引率
9.00%
发文量
48
审稿时长
3.3 months
期刊介绍: Archives of Pharmacal Research is the official journal of the Pharmaceutical Society of Korea and has been published since 1976. Archives of Pharmacal Research is an interdisciplinary journal devoted to the publication of original scientific research papers and reviews in the fields of drug discovery, drug development, and drug actions with a view to providing fundamental and novel information on drugs and drug candidates.
期刊最新文献
Saponins as potential novel NLRP3 inflammasome inhibitors for inflammatory disorders. Modulating versatile pathways using a cleavable PEG shell and EGFR-targeted nanoparticles to deliver CRISPR-Cas9 and docetaxel for triple-negative breast cancer inhibition. Ginsenoside Rg3 activates the immune function of CD8+ T cells via circFOXP1-miR-4477a-PD-L1 axis to induce ferroptosis in gallbladder cancer. Potential effects of a human milk oligosaccharide 6'-sialyllactose on angiotensin II-induced aortic aneurysm via p90RSK/TGF-β/SMAD2 signaling pathway. Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1