ObjectiveTo investigate the therapeutic effect of Qingmei compound on acute gouty arthritis （AGA） in rats and preliminarily clarify its mechanism. MethodForty male SD rats were randomly divided into a blank group， a model group， a colchicine group （0.3 mg·kg^-1）， and low- and high-dose Qingmei compound groups （200 and 400 mg·kg^-1）， with eight rats in each group. The AGA model was induced by injecting 50 g·L^-1 monosodium urate （MSU） into the ankle joint of the rats except those in the blank group. The ankle swelling index was measured before and 6， 24， and 48 h after modeling. The pathological changes in the joint tissues of AGA rats were observed by hematoxylin-eosin （HE） staining. The expression of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the joint tissues of rats was detected by immunohistochemistry. The protein expression of NOD-like receptor protein 3 （NLRP3） pathway and key proteins in the joint tissues of rats was detected by Western blot. ResultCompared with the blank group， the model group showed increased ankle swelling index， synovial hyperplasia， and inflammatory infiltration， and up-regulated expression of IL-1β， TNF-α， and NLRP3 proteins in the ankle joint and the ratio of Caspase-1 shear body to Caspase-1 precursor protein （Caspase-1 p20/Caspase-1） （P<0.01）. Compared with the model group， the Qingmei compound groups showed reduced ankle swelling index of AGA rats， especially the low-dose Qingmei compound group （P<0.01）. Meanwhile， Qingmei compound inhibited synovial hyperplasia and inflammatory infiltration （P<0.01） and reduced the levels of IL-1β， TNF-α， and NLRP3 proteins and Caspase-1 p20/Caspase-1 in joint tissues （P<0.01）. ConclusionQingmei Compound can significantly alleviate the joint swelling and inflammatory infiltration of AGA， and its mechanism may be related to the inhibition of the NLRP3 signaling pathway.