Icariin (ICA) has anti‐inflammatory effects in some diseases, but its role in gouty arthritis (GA) is not clear. This study investigated the effects of ICA in monosodium urate (MSU)‐induced GA rat models. GA rat models were induced by MSU, and co‐treated with ICA of low‐dose (20 mg/kg), medium‐dose (40 mg/kg), and high‐dose (80 mg/kg), respectively. The ankle swelling rates, haematoxylin‐eosin (HE) staining changes, inflammatory factors (interleukin (IL)‐1β, IL‐6, tumour necrosis factor‐α (TNF‐α)) and prostaglandin E2 (PGE₂) levels in synovial tissues were detected. The antioxidants levels in rat serum, and NF‐κB pathway‐related proteins and NALP3 inflammasome expressions in synovial tissues were also analysed. In cell experiments, chondrocytes were co‐treated with different concentrations of ICA (1, 5, 10 μmol/L) on the basis of MSU. The activities and inflammatory cytokines, hydroxyproline (Hyp) and glycosaminogly (GAG) expressions in chondrocytes were measured. In rat experiments, MUS increased the ankle swelling rates, promoted inflammatory cells infiltration, and increased IL‐1β, IL‐6, TNF‐α, PGE₂ levels in synovial tissues, which were all alleviated by ICA. Moreover, ICA also suppressed nuclear translocation of NF‐κB pathway‐related proteins and reduced the expression of NALP3 inflammasome in rat models. As for cell experiments, ICA decreased the activity, inflammatory cytokines and GAG levels, and suppressed nuclear translocation of NF‐κB pathway‐related proteins of MSU‐treated chondrocytes. In general, medium and high concentrations of ICA showed good effects. ICA has an inhibitory effect in MSU‐induced rat GA models through NF‐κB/NALP3 pathway, which may provide a direction for the treatment of GA.

中文翻译：

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Icariin通过NF-κB/ NALP3途径缓解MSU诱导的大鼠GA模型

伊卡林（ICA）在某些疾病中具有抗炎作用，但其在痛风性关节炎（GA）中的作用尚不清楚。这项研究调查了ICA在尿酸一钠（MSU）诱导的GA大鼠模型中的作用。用MSU诱导GA大鼠模型，并分别与低剂量（20 mg / kg），中剂量（40 mg / kg）和高剂量（80 mg / kg）的ICA共同治疗。踝关节肿胀率，苏木精-伊红（HE）染色变化，炎性因子（白介素（IL）-1β，IL-6，肿瘤坏死因子-α（TNF-α））和前列腺素E2（PGE ₂检测滑膜组织中的水平。还分析了大鼠血清中的抗氧化剂水平，滑膜组织中的NF-κB通路相关蛋白和NALP3炎性小体表达。在细胞实验中，在MSU的基础上，将软骨细胞与不同浓度的ICA（1、5、10μmol/ L）共同处理。测量软骨细胞的活性和炎性细胞因子，羟脯氨酸（Hyp）和糖胺聚糖（GAG）的表达。在大鼠实验中，MUS可增加踝关节肿胀率，促进炎性细胞浸润并增加IL-1β，IL-6，TNF-α，PGE ₂滑膜组织中的血红蛋白水平可以通过ICA缓解。此外，ICA还抑制了NF-κB通路相关蛋白的核易位，并降低了大鼠模型中NALP3炎性小体的表达。至于细胞实验，ICA降低了MSU处理的软骨细胞的活性，炎性细胞因子和GAG水平，并抑制了NF-κB通路相关蛋白的核易位。通常，中等和高浓度的ICA表现出良好的效果。ICA通过NF-κB/ NALP3途径在MSU诱导的大鼠GA模型中具有抑制作用，这可能为GA的治疗提供指导。