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This research investigates the therapeutic effects of Naru Sanwei Pills on gout and clarifies their anti-inflammatory and uric acid-lowering mechanisms.

April 19, 2026Journal of Inflammation Research0 citationsOpen Access

Dual Mechanisms of Naru Sanwei Pills in Gout: NLRP3 Inflammasome Inhibition and Uric Acid Regulation

ZLZ LIU ACAichun Chu SGShupei Gao

Key Points

This research investigates the therapeutic effects of Naru Sanwei Pills on gout and clarifies their anti-inflammatory and uric acid-lowering mechanisms.
Evaluated Naru Sanwei Pills effects in an MSU-induced gouty arthritis model over 5 days.
Conducted transcriptomic analysis to understand mechanisms of action.
Identified chemical constituents and potential targets using UPLC-Q/TOF-MS and network pharmacology.
Validated findings in vivo through various animal models, including gene-deficient mice.
Assessed uric acid-lowering effects in a hyperuricemic nephropathy model over 28 days.
Naru Sanwei Pills significantly reduced joint swelling and pain in gouty arthritis models.
Decreased IL-1β and TNF-α levels demonstrated anti-inflammatory effects.
Naru-3 reversed aberrant NOD-like receptor and NF-κB pathway activations.
The treatment lowered serum uric acid levels and improved renal injury in hyperuricemic mice.
Mechanistically, Naru-3 inhibited NLRP3 inflammasome activation, confirmed by studies in deficient mice.

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. Keywords: Naru Sanwei Pills, hyperuricemic nephropathy, gouty arthritis, anti-inflammatory, NLRP3 inflammasome

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