Sunflower Receptacle Extract Alleviates Acute Gouty Arthritis via HMGB1-TLR4-NLRP3 Inflammatory Pathway

Background/Objectives: Acute gouty arthritis (AGA) is an auto-inflammatory disorder characterized by dysregulated innate immune activation and overactive NOD-like receptor family pyrin domain-containing 3 (NLRP3)/Toll-like receptor 4 (TLR4) inflammatory signaling. While adverse effects limit current therapies, the mechanism by which sunflower receptacle extract (SPE) alleviates gout remains unclear.

Methods

This study investigated the anti-inflammatory mechanism of SPE in a male SPF-grade SD rat model of AGA induced by intra-articular monosodium urate crystals. Rats were orally administered SPE or colchicine, and ankle joint swelling, synovial histopathology, serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β), and interleukin-6 (IL-6), and synovial protein expression were assessed. Western blotting was used to assess the expression of the high-mobility group box 1 (HMGB-1), TLR4, and mitogen-activated protein kinase (MAPK) signaling pathways, as well as the activation of NLRP3.