ArticleAntioxidants (Basel, Switzerland)2024
Indole-3-Carboxaldehyde Alleviates LPS-Induced Intestinal Inflammation by Inhibiting ROS Production and NLRP3 Inflammasome Activation.
Article in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Gut microbiota metabolites in the immunoregulation of enteritis: research progress.Frontiers in immunology · 2025Pooled it
- Microbiome-driven alterations in tryptophan metabolism contribute to behavioral comorbidities in the Muc2 knockout mouse model of chronic colitis.Gut microbes · 2026Article
- Ethanol extract of Astragali Radix inhibits M1 macrophage polarization to alleviate ulcerative colitis by promoting Lactobacillus reuteri-produced indole-3-carboxaldehyde and formononetin.Chinese medicine · 2026Article
- Decoding the gut microbiota-mitochondrial-inflammasome axis in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- Indole-3-aldehyde Preserves Gingival Epithelial Barrier Structure and Function Via AhR/Nrf2 Signaling Pathway.Inflammation · 2026Article
- Gut microbiota-derived tryptophan metabolite indole-3-carboxaldehyde enhances intestinal barrier function via aryl hydrocarbon receptor/AMP-activated protein kinase signaling activation.Animal bioscience · 2026Article
- Spermidine protects against ETEC-induced intestinal injury by reshaping the gut microbiota and activating the AhR/IL-22 axis.Frontiers in microbiology · 2026Article
- Fecal Metabolomic Insights into Memory-Associated Pathways Modulated byAntioxidants (Basel, Switzerland) · 2026Article
- PANoptosis links gut dysbiosis to obstructive sleep apnea-associated atherosclerosis: a gut-vascular inflammatory axis.Frontiers in immunology · 2026Review
- Metabolic regulation of gut barrier integrity in IBD: protein, lipid, and carbohydrate pathways.Frontiers in nutrition · 2026Review
- Therapeutic potential of nutritional aryl hydrocarbon receptor ligands for respiratory syncytial virus infection: a mini review.Frontiers in microbiology · 2026Review
- Plant-Derived Extracellular-Vesicle-Like Particles: Immune Regulation and Disease Therapy.Research (Washington, D.C.) · 2026Review
- Gut microbiota-derived tryptophan metabolites: molecular mechanisms, nutritional strategies and implications for swine health.Frontiers in veterinary science · 2026Review
- Aryl hydrocarbon receptor: a potential target for natural products in the treatment of inflammatory bowel disease.Frontiers in immunology · 2026Review
- Integrative serum metabolite prioritization and functional screening identify N-acetyl-L-glutamine as a protective candidate in premature ovarian insufficiency.Frontiers in genetics · 2026Article
- A "One-Stone-Three-Birds" Inspired Nanoplatform for Multitargeted Ulcerative Colitis Therapy via Combined Aryl Hydrocarbon Receptor Activation and Reactive Oxygen Species Scavenging.Biomaterials research · 2026Article
- Dehydroandrographolide Alleviates Oxidative Stress, Inflammatory Response, and Pyroptosis in DSS-Induced Colitis Mice by Modulating Nrf2 Signaling Pathway.Biomolecules · 2025Article
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3 authors.
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Abstract
Indole-3-carboxaldehyde (IAld) is a tryptophan (Trp) metabolite derived from gut microbiota, which has a potential protective effect on intestinal inflammatory diseases. Abnormal activation of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is an important cause of intestinal inflammation. However, the effect and mechanism of IAld on NLRP3 inflammasome activation remain unclear. Here, we found that IAld inhibited the activation of the NLRP3 inflammasome in intestinal epithelial cells, and effectively prevented intestinal epithelial barrier injury caused by lipopolysaccharide (LPS) stimulation. Mechanistically, we demonstrated that IAld activated the aryl hydrocarbon receptor (AhR), subsequently prevented reactive oxygen species (ROS) production, maintained mitochondrial membrane potential, and blocked the NF-κB/NLRP3 inflammatory pathway in intestinal epithelial cells. Also, the AhR-specific inhibitor CH-223191 effectively blocked the IAld-induced NLRP3 inhibition and intestinal epithelial barrier repairment. In addition, in vivo results showed that IAld prevented pro-inflammatory mediator production and intestinal inflammatory damage in LPS-induced mice, which is related to AhR activation and NLRP3 inflammasome inhibition. Collectively, our study unveiled that IAld is an effective endogenous antioxidant and suggested the AhR as a potential treatment target for NLRP3-induced intestinal inflammatory diseases.
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