The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NF kappa B and macrophage release of IL-1 beta

The effects and mechanisms of the citrus flavonoid naringenin were investigated in a mouse model of gout arthritis induced by intra-articular injection of monosodium urate crystals (MSU). Mice were treated with naringenin (16.7-150 mg/kg, per oral) 1 h before MSU (100 mu g/kg, i.a.) stimulus. MSU induced joint pain and edema, which were inhibited by naringenin at the dose of 150 mg/kg, without inducing liver and kidney toxicity. Naringenin inhibited MSU-induced histopathological changes, leukocyte recruitment, cytokine production, oxidative stress, NF kappa B activation, NLRP3 inflammasome components mRNA expression, and IL-1 beta maturation in cultured macrophages. The present data support the therapeutic applicability of naringenin in the treatment of gout arthritis.