Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.

Abstract

Gouty arthritis (GA) is a metabolic inflammatory disorder characterized by the deposition of monosodium urate crystals. Although conventional treatments like colchicine can relieve symptoms, they come with several limitations, such as gastrointestinal side effects, hepatorenal toxicity, and poor target specificity. In contrast, natural products, known for their multi-pathway and multi-target properties, present distinct advantages and significant potential for intervening in GA. The primary pathological mechanism of GA involves the overactivation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, making its regulation a promising therapeutic approach. However, there is currently a lack of comprehensive reviews on how natural products target the NLRP3 inflammasome. Additionally, existing studies have not sufficiently classified or integrated the mechanisms involved in transcriptional and translational regulation during the priming phase, post-translational modifications, and the various pathways active during the activation phase. This article aims to address these gaps through a systematic literature review, providing an in-depth analysis of the molecular mechanisms by which natural products alleviate GA by targeting the NLRP3 inflammasome. It also critically examines the major challenges in current translational research, with the objective of offering a solid theoretical foundation and practical strategies for developing novel, effective anti-inflammatory drugs and expediting the clinical application of natural products for GA treatment.