Baicalein links macrophage M2 polarization with reduced synovial inflammation to alleviate gouty arthritis

ObjectiveGouty arthritis (GA) is an inflammatory disease caused by abnormal uric acid metabolism, with its pathological mechanism involving inflammatory cell infiltration and abnormal expression of pro-inflammatory factors. Monosodium urate (MSU) crystals activate the NLRP3 inflammasome, promoting the abnormal release of pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), as well as the expression of mediators like monocyte chemoattractant protein-1 (MCP-1) and high mobility group box 1 (HMGB1), thereby amplifying local inflammatory responses. Additionally, MSU crystals activate Toll-like receptors (TLRs) and their downstream signaling pathways, including nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPK), driving the aggregation of inflammatory cells such as neutrophils and macrophages into the joint cavity, mediating synovial tissue damage, and causing oxidative stress imbalance.