ArticleLaboratory investigation; a journal of technical methods and pathology2018
NLRP3 inflammasome inhibition ameliorates tubulointerstitial injury in the remnant kidney model.
Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Function of molecular-weight-optimized Astragalus polysaccharides in cisplatin-caused acute kidney injury: mechanisms centered on gut microbiota regulation and precise treatment approaches.Frontiers in microbiology · 2026Review
- Uric Acid and Preeclampsia: Pathophysiological Interactions and the Emerging Role of Inflammasome Activation.Antioxidants (Basel, Switzerland) · 2025Review
- Association between the ratio of triglyceride to high-density lipoprotein cholesterol (TG/HDL-c) and chronic kidney disease risk: a large-scale cross-sectional study in a Chinese population.Frontiers in medicine · 2025Article
- Renal interstitial fibrotic assessment using non-Gaussian diffusion kurtosis imaging in a rat model of hyperuricemia.BMC medical imaging · 2024Article
- Erythrocyte membrane biomimetic EGCG nanoparticles attenuate renal injury induced by diquat through the NF-κB/NLRP3 inflammasome pathway.Frontiers in pharmacology · 2024Article
- Adenine model of chronic renal failure in rats to determine whether MCC950, an NLRP3 inflammasome inhibitor, is a renopreventive.BMC nephrology · 2023Article
- Adipolin protects against renal injury via PPARα-dependent reduction of inflammasome activation.iScience · 2023Article
- Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.Biochemistry and biophysics reports · 2023Review
- Editorial: Global excellence in renal pharmacology 2022: Central and South America.Frontiers in pharmacology · 2023Article
- Acute Kidney Injury and Gut Dysbiosis: A Narrative Review Focus on Pathophysiology and Treatment.International journal of molecular sciences · 2022Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Protein-Bound Uremic Toxins Induce Reactive Oxygen Species-Dependent and Inflammasome-Mediated IL-1β Production in Kidney Proximal Tubule Cells.Biomedicines · 2021Article
- Promise of the NLRP3 Inflammasome Inhibitors in In Vivo Disease Models.Molecules (Basel, Switzerland) · 2021Review
- The Role of the Inflammasome in Heart Failure.Frontiers in physiology · 2021Review
- Renal Inflammation and Innate Immune Activation Underlie the Transition From Gentamicin-Induced Acute Kidney Injury to Renal Fibrosis.Frontiers in physiology · 2021Article
- Antituberculosis Drugs (Rifampicin and Isoniazid) Induce Liver Injury by Regulating NLRP3 Inflammasomes.Mediators of inflammation · 2021Article
- Cardio-renal protective effect of the xanthine oxidase inhibitor febuxostat in the 5/6 nephrectomy model with hyperuricemia.Scientific reports · 2020Article
- NF-κB System Is Chronically Activated and Promotes Glomerular Injury in Experimental Type 1 Diabetic Kidney Disease.Frontiers in physiology · 2020Article
- Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury.BioMed research international · 2020Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies suggest that NLRP3 inflammasome activation is involved in the pathogenesis of chronic kidney disease (CKD). Allopurinol (ALLO) inhibits xanthine oxidase (XOD) activity, and, consequently, reduces the production of uric acid (UA) and reactive oxygen species (ROS), both of which can activate the NLRP3 pathway. Thus, ALLO can contribute to slow the progression of CKD. We investigated whether inhibition of XOD by ALLO reduces NLRP3 activation and renal injury in the 5/6 renal ablation (Nx) model. Adult male Munich-Wistar rats underwent Nx and were subdivided into the following two groups: Nx, receiving vehicle only, and Nx + ALLO, Nx rats given ALLO, 36 mg/Kg/day in drinking water. Rats undergoing sham operation were studied as controls (C). Sixty days after surgery, Nx rats exhibited marked albuminuria, creatinine retention, and hypertension, as well as glomerulosclerosis, tubular injury, and cortical interstitial expansion/inflammation/fibrosis. Such changes were accompanied by increased XOD activity and UA renal levels, associated with augmented heme oxigenase-1 and reduced superoxide dismutase-2 renal contents. Both the NF-κB and NLRP3 signaling pathways were activated in Nx. ALLO normalized both XOD activity and the parameters of oxidative stress. ALLO also attenuated hypertension and promoted selective tubulointerstitial protection, reducing urinary NGAL and cortical interstitial injury/inflammation. ALLO reduced renal NLRP3 activation, without interfering with the NF-κB pathway. These observations indicate that the tubulointerstitial antiinflammatory and antifibrotic effects of ALLO in the Nx model involve inhibition of the NLRP3 pathway, and reinforce the view that ALLO can contribute to arrest or slow the progression of CKD.
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