Background. Cyr61 is considered a novel proinflammatory factor. Gouty arthritis (GA) is a self-limited inflammatory reaction caused by monosodium urate (MSU) crystals. In this study, we assessed the role of Cyr61 in the inflammatory process of GA. Methods. We investigated the expression of Cyr61 in MSU-induced rat gout models and MSU-stimulated rat fibroblast-like synovial (FLS) cells. After inhibiting the expression of Cyr61, levels of IL-1β, TNF-α, and IL-6 were detected by ELISA, qPCR, western blot, and immunohistochemical methods. We probed the downstream NF-κB signaling pathway using the NF-κB inhibitor PDTC, and levels of NF-κB and p-NF-κB were detected by western blot and qPCR. Results. Our results demonstrate that Cyr61 plays a potent role in the formation of local inflammation in vitro and in vivo. Cyr61 was highly expressed in synovial tissues of gout models, and the expression of Cyr61 protein was also significantly increased in MSU-stimulated FLS cells. Cyr61 promoted MSU-induced acute inflammation via the NF-κB signaling pathway. Conclusions. Our study has revealed that Cyr61 is an important regulatory factor for the initiation of inflammation in GA. The high expression of Cyr61 protein can induce synovial cells to produce many inflammatory cytokines, such as IL-1β, TNF-α, and IL-6, partly in an NF-κB-dependent manner. Thus, inhibition of Cyr61 could be a new target and strategy for the prevention and treatment of GA.

中文翻译：

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Cyr61 促进大鼠痛风性关节炎模型的炎症。

背景。Cyr61 被认为是一种新的促炎因子。痛风性关节炎 (GA) 是由尿酸单钠 (MSU) 结晶引起的自限性炎症反应。在这项研究中，我们评估了 Cyr61 在 GA 炎症过程中的作用。方法。我们研究了 Cyr61 在 MSU 诱导的大鼠痛风模型和 MSU 刺激的大鼠成纤维细胞样滑膜 (FLS) 细胞中的表达。抑制Cyr61表达后，ELISA、qPCR、western blot、免疫组化等方法检测IL- 1β、TNF - α 、IL-6水平。我们使用 NF- κB抑制剂 PDTC探测下游 NF-κB信号通路，以及 NF- κB和 p-NF- κ的水平B通过蛋白质印迹和qPCR检测。结果。我们的研究结果表明，Cyr61 在体外和体内局部炎症的形成中发挥着重要作用。Cyr61在痛风模型的滑膜组织中高表达，并且在MSU刺激的FLS细胞中Cyr61蛋白的表达也显着增加。Cyr61 通过 NF- κB信号通路促进 MSU 诱导的急性炎症。结论。我们的研究表明，Cyr61 是 GA 炎症起始的重要调节因子。Cyr61 蛋白的高表达可诱导滑膜细胞产生许多炎性细胞因子，如 IL-1 β、TNF - α和 IL-6，部分在 NF- κB依赖方式。因此，抑制 Cyr61 可能成为预防和治疗 GA 的新靶点和策略。