ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021
Uric acid drives intestinal barrier dysfunction through TSPO-mediated NLRP3 inflammasome activation.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- 6'‑O‑Caffeoylarbutin attenuates experimental hyperuricemia by regulating renal and intestinal urate transport, intestinal barrier integrity, and gut microbiota.Molecular medicine reports · 2026Article
- Multi-target effects of Limosilactobacillus reuteri RE225 on hyperuricemia through xanthine oxidase inhibition, nucleoside degradation, gut microbiota modulation, and renal TLR4-NF-κB suppression.Journal of the science of food and agriculture · 2026Article
- Isobavachin Attenuates Renal and Cardiac Injury in Chronic Hyperuricemia via Modulation of NF-κB and NLRP3 Signaling Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Smart contact lens-trained digital twin for device-free personalized uric acid prediction.Science advances · 2026Article
- Identification and Validation of Key Purine Metabolism-Related Genes in Ulcerative Colitis Using Bioinformatics and Machine Learning.Journal of inflammation research · 2026Article
- Serum uric acid to high‑density lipoprotein cholesterol ratio as a novel predictor of diabetic nephropathy: a cross‑sectional analysis of NHANES 2011-2018.Clinical and experimental medicine · 2025Article
- Cathepsin B-dependent glycolysis contributes to reduced renal uric acid excretion in hyperuricemia.Communications biology · 2025Article
- Uricase deficiency in rats results in a variety of metabolic disorders, addition to gouty nephropathy.PloS one · 2025Article
- Rewiring of Uric Acid Metabolism in the Intestine Promotes High-Altitude Hypoxia Adaptation in Humans.Molecular biology and evolution · 2024Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- The Role of Hyperuricemia in Cardiac Diseases: Evidence, Controversies, and Therapeutic Strategies.Biomolecules · 2024Review
- Hyperuricemia Increases the Risk of Postoperative Recurrence in Chinese Patients with Chronic Rhinosinusitis.Journal of inflammation research · 2024Article
- ProbioticInternational journal of molecular sciences · 2024Article
- Bilosomes and Biloparticles for the Delivery of Lipophilic Drugs: A Preliminary Study.Antioxidants (Basel, Switzerland) · 2023Article
- Prevalence and Risk Factors of Metabolic-Associated Fatty Liver Disease Among Hospital Staff.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Article
- Folic acid and zinc improve hyperuricemia by altering the gut microbiota of rats with high-purine diet-induced hyperuricemia.Frontiers in microbiology · 2022Article
- Translocator Protein 18 kDa (TSPO) as a Novel Therapeutic Target for Chronic Pain.Neural plasticity · 2022Review
- Koumine Suppresses IL-1β Secretion and Attenuates Inflammation Associated With Blocking ROS/NF-κB/NLRP3 Axis in Macrophages.Frontiers in pharmacology · 2020Article
- Serum metabolic biomarkers associated with self-reported chronic rhinosinusitis: a population-based cross-sectional study from the KNHANES.Brazilian journal of otorhinolaryngologyArticle
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimIntestinal epithelial dysfunction is the foundation of various intestinal and extra-intestinal diseases, while the effects and mechanism of uric acid on the intestinal barrier are little known. TSPO has been shown to be related to the generation of ROS and is involved in regulating inflammation, whether uric acid drives intestinal epithelial dysfunction through TSPO-mediated NLRP3 inflammasome activation is unknown.
methodsUOX gene knockout mouse (UOX-/-) were used for models of hyperuricemia. Fluorescein isothiocyanate (FITC)-labeled dextran was used to assess in vivo intestinal permeability. Serum lipopolysaccharide (LPS) and culture supernatants IL-1β were measured using ELISA Kit. IEC-6 exposed to different concentrations of uric acid was used for in vitro experiment. Protein content and mRNA were assessed using Western blotting and Q-PCR, respectively. Intracellular ROS was determined using flow cytometry and fluorescence microscope. Mitochondrial membrane potential was detected on an immunofluorescence. Small interfering RNA transfection was used to assess the interaction between translocator protein (TSPO) and NLRP3 inflammasome. N-acetyl-L-cysteine (NAC) was used as ROS scavenger.
resultsOur results showed that hyperuricemia mice were characteristic by increased intestinal permeability. Hyperuricemia upregulated TSPO, increased production of ROS and activated NLRP3 inflammasome, which resulted in lower expression of occludin and claudin-1. In vitro, we showed that soluble uric acid alone increased the expression of TSPO, depolarized mitochondrial membrane potential, increased ROS release and activated NLRP3 inflammasome, which further reduced the expression of occludin and claudin-1. Silencing TSPO suppressed NLRP3 inflammasome activation and increased expression of claudin-1 and occludin, which was accompanied by lower levels of ROS. Scavenging ROS also significantly inhibited NLRP3 inflammasome activation without change of TSPO, indicating that TSPO-mediated NLRP3 inflammasome activation was dependent on ROS.
conclusionsIn conclusion, uric acid drives intestinal barrier dysfunction through TSPO-mediated NLRP3 inflammasome.
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