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。

IF 6.9 3区 医学 Q1 CHEMISTRY, MEDICINAL
Xinyan Qu, Yingying Song, Qingjun Li, Qi Xu, Yanru Li, Huimin Zhang, Xuemei Cheng, Charles R. Mackay, Quanbo Wang, Wei Liu
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引用次数: 0

摘要

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。

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

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

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

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.

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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.
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