ArticleJournal of inflammation research2026
Dual Mechanisms of Naru Sanwei Pills in Gout: NLRP3 Inflammasome Inhibition and Uric Acid Regulation.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Gout is a metabolic inflammatory disorder driven by monosodium urate (MSU) crystal-induced activation of the NLRP3 inflammasome and frequently accompanied by hyperuricemia-related renal injury. This study aimed to investigate the therapeutic effects of Naru Sanwei Pills (Naru-3) on gout and to elucidate the underlying anti-inflammatory and uric acid-lowering mechanisms. Methods: The anti-gout effects of Naru-3 were initially evaluated in an MSU-induced acute gouty arthritis model (5 days), followed by transcriptomic analysis to investigate the underlying mechanisms. The chemical constituents and potential targets of Naru-3 were subsequently identified through UPLC-Q/TOF-MS, network pharmacology, and molecular docking. Key findings were validated in vivo, including the anti-inflammatory effects of representative compounds in an air pouch model and mechanistic confirmation using gene-deficient mice. Additionally, a potassium oxonate-induced hyperuricemic nephropathy model (28 days) was employed to assess the uric acid-lowering and renoprotective effects. Results: Naru-3 markedly alleviated MSU-induced gouty arthritis by reducing joint swelling, pain hypersensitivity, inflammatory cell infiltration, and IL-1β and TNF-α production. Transcriptomic and pathway enrichment analyses revealed that Naru-3 reversed aberrant activation of the NOD-like receptor and NF-κB signaling pathways. Integrated network pharmacology identified multiple active compounds targeting gout-related proteins, several of which showed strong binding affinity to NLRP3-associated proteins and significant anti-inflammatory activity in vivo. Mechanistically, Naru-3 inhibited NLRP3 inflammasome activation, as confirmed by diminished efficacy in NLRP3- and caspase-1-deficient mice. Furthermore, Naru-3 significantly reduced serum uric acid levels and ameliorated renal injury in hyperuricemic mice by suppressing xanthine oxidase and adenosine deaminase activities and regulating renal urate transporters. Conclusion: Naru-3 exerts dual therapeutic effects against gout by inhibiting NLRP3 inflammasome-mediated inflammation and restoring uric acid homeostasis, supporting its potential as a multitarget therapy for gout and hyperuricemia-related renal injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.