色氨酸代谢产物调控肠道氧化应激研究进展

doi:10.11843/j.issn.0366-6964.2026.01.005

Abstract

Abstract:

The gastrointestinal tract is not only a place where nutrients digest， absorb and metabolize， but also serves as both a primary source and a major target of reactive oxygen species （ROS）. Intestinal health is a cornerstone of animal growth and a critical determinant of livestock production efficiency. Tryptophan， an essential amino acid， is metabolized by both host cells and gut microbiota into various bioactive compounds， such as indole， kynurenine and 5-hydroxytryptamine. These metabolites act as endogenous ligands to regulate intestinal oxidative stress and inflammatory damage. This review summarizes the host and microbial pathways of intestinal tryptophan metabolism， explores the physiological functions of tryptophan metabolites in modulating oxidative stress and tissue repair， and discusses the role of microbial tryptophan metabolism in potential nutritional interventions，including probiotics and nutritional supplements. These findings aim to inform research on nutritional strategies for managing gut health.

Key words: intestine, oxidative stress, tryptophan metabolism, intestinal microorganisms, nutritional regulation

CLC Number:

S852.2

MENG Yunlong, DENG Yuankun, TAN Bi’e, WANG Jing. Research Progress on Tryptophan Metabolites in Alleviating Intestinal Oxidative Stress[J]. Acta Veterinaria et Zootechnica Sinica, 2026, 57(1): 46-57.

Figures/Tables 2

Fig.1

Table 1

Tryptophan metabolite binding receptors modulate intestinal oxidative stress and damage repair"

受体 Receptor	代谢产物 Metabolites	调节方式 Regulatory methods	参考文献 Reference
芳香烃受体 Aryl hydrocarbon receptor	犬尿氨酸	激活AhR下游Foxp3转录因子表达，诱导Treg细胞表达；缓解氧化应激造成的Treg细胞损失出现的免疫失衡，阻止肠道炎症发生	［26，51］
	AA	参与Nrf2信号转录途径，诱导HO-1表达，调控AhR抗氧化平衡	［52］
	IPA	激活AhR调节肠道T细胞活性，减少炎症因子TNF-α、IL-1β以及IL-6表达，调控肠道免疫屏障	［32］
	色胺	激活AhR之后，减少Th17细胞以及RORγT细胞的数量，增加Treg细胞水平，减少炎症发生	［49］
	IALD	可以抑制肌动蛋白激活，维持顶部连接复合物表达，调控肠道上皮通透性；结合AhR之后，诱导下游IL-22的表达，IL-22激活STAT通路抑制肠道炎症	［46⁃47］
	IPyA	抑制肌动蛋白激活，维持顶部连接复合物表达，调控肠道上皮通透性	［46］
	ILA	与AhR结合抑制炎症细胞因子IL-8以及TNF-α表达，上调IL-22的表达，缓解肠道炎症	［48］
	IAA	调控Foxp3信号通路，诱导Treg细胞的表达；结合AhR后，促进下游CYP1A1、CYP1B1和RegIIIγ表达，与Occludin和ZO-1的表达呈正相关；显著抑制炎症细胞因子IL-1β、TNF-α以及IL-6的表达，减轻炎症反应；激活AhR并通过NF-κB/MAPK信号通路减少Th17细胞水平，降低Th17细胞相关炎症因子IL-17、IL-6以及RORγt的表达；提高结肠IL-22分泌水平，并上调肠道紧密连接蛋白表达以缓解肠道损伤	［50，63，65⁃67］
5-羟色胺受体 6-5-Hydroxytryptamine receptor	5-HT	与5-HTR结合后，招募免疫细胞到肠道损伤或炎症部位，促进细胞因子、黏附因子释放；与5-HT₄R结合，减少单核细胞TNF-α的释放	［54］
孕烷X受体 Pregnane X receptor	IPA	激活PXR之后，抑制TLR4/NF-κB信号通路，减少促炎细胞因子的释放，缓解炎症反应；激活PXR之后上调肠道紧密连接蛋白的表达、下调肠道中TNF-α表达，降低肠道通透性	［56⁃57］
褪黑素受体 Melatonin receptor	褪黑素	可直接进入线粒体内，清除线粒体中的ROS；提升抗氧化酶SOD、CAT等酶的活性，减少ROS水平；上调Nrf2信号通路，增加HO-1表达，增强肠道抗氧化能力；减少免疫细胞向炎症部位移动，降低IL-1β和TNF-β水平，抑制NLRP3表达，减轻炎症反应	［58⁃59］

Table 1

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Research Progress on Tryptophan Metabolites in Alleviating Intestinal Oxidative Stress

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