This study preliminarily investigated the mechanism by which Sanghuangporus sanghuang polysaccharide (SHP) alleviates acute gouty arthritis (AGA) through regulating the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. SHP was isolated and purified by water extraction and alcohol precipitation combined with gel chromatography. Some techniques were used to characterize SHP, including high-performance liquid chromatography coupled with ultraviolet detection, refractive index detection, multi-angle laser light scattering (HPLC-UV-RI-MALLS), scanning electron microscopy (SEM) and ion exchange chromatography. These techniques were used to analyze its purity, molecular weight distribution, and monosaccharide composition. An AGA mouse model was established by injecting of monosodium urate (MSU) crystals into male C57BL/6 mice. The mice were then randomly divided into six groups: normal control group, model group, positive control group (allopurinol, 10 mg/kg), SHP low-dose group (50 mg/kg), medium-dose group (150 mg/kg), and high-dose group (250 mg/kg), with an intervention period of 4 weeks. The results showed that SHP was a homogeneous polysaccharide. Its weight-average molecular weight was 17.15 kDa, polysaccharide content was 75.14%, protein content was 12.15%. It was mainly composed of glucose (41.62%), galactose (27.48%), fucose (17.31%), and mannose (9.40%). SHP significantly reduced joint swelling, improved synovial tissue pathological damage, and inhibited inflammatory cell infiltration in a dose-dependent manner. Immunofluorescence and ELISA results indicated that SHP inhibited NLRP3 inflammasome activation, down-regulated the protein expression of cysteinyl aspartate-specific proteinase 1 (Caspase-1) and interleukin-1β (IL-1β), and significantly reduced the levels of tumor necrosis factor-α (TNF-α), IL-6 and IL-1β .The high-dose group showed decreases of 84.28%, 78.2%, and 78.4% compared with the model group, respectively (P<0.05), suggesting that it exerts anti-inflammatory effects by regulating the NLRP3/Caspase-1/IL-1β signaling pathway. This study systematically evaluated the protective effect of SHP against AGA, preliminarily revealed the molecular mechanism by which SHP antagonizes AGA injury via targeting the NLRP3/Caspase-1/IL-1β signaling pathway, and provided new ideas for the development of fungal drugs.