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 µg/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, NFκB activation, NLRP3 inflammasome components mRNA expression, and IL-1β maturation in cultured macrophages. The present data support the therapeutic applicability of naringenin in the treatment of gout arthritis.

在关节内注射尿酸一钠晶体（MSU）诱发的痛风性关节炎小鼠模型中研究了柑橘类黄酮柚皮苷的作用及其机制。在MSU（100 µg / kg，ia）刺激之前1小时，用柚皮素（16.7–150 mg / kg，每次口服）治疗小鼠。MSU引起关节疼痛和水肿，在150 mg / kg的剂量下柚皮素抑制了关节疼痛和水肿，而没有引起肝肾毒性。柚皮苷抑制MSU诱导的组织病理学变化，白细胞募集，细胞因子生成，氧化应激，NFκB活化，NLRP3炎性小体成分mRNA表达以及培养的巨噬细胞中IL-1β的成熟。本数据支持柚皮苷在痛风性关节炎的治疗中的应用性。