【摘要】 目的 研究单叶铁线莲总皂苷（Ts CH）抑制滑膜细胞激活的作用及可能机制。方法 细胞实验：用不同浓度的Ts CH预孵育滑膜细胞12 h后用肿瘤坏死因子-α(TNF-α)处理。CCK-8和流式细胞仪检测细胞增殖和细胞周期；Transwell检测细胞迁移；ELISA法检测细胞培养上清液中IL-1β和IL-18的水平；Western blot法检测NLRP3、caspase-1、MMP2和MMP9的表达。动物实验：建立胶原诱导的大鼠风湿性关节炎模型，Ts CH灌胃处理4周后评价关节炎指数评分、足趾体积以及厚度；检测大鼠关节组织中IL-1β、IL-18、NLRP3和Caspase-1的表达。结果细胞实验结果表明Ts CH能抑制TNF-α诱导的滑膜细胞增殖以及迁移，同时抑制IL-1β、IL-18、NLRP3、Caspase-1、MMP2和MMP9蛋白表达水平的升高。动物实验结果表明Ts CH能降低关节炎大鼠的关节炎指数评分、减小足趾容积和足趾厚度，以及降低关节组织中TNF-α、IL-18、IL-1β、NLRP3、Caspase-1的表达水平。结论 Ts CH对类风湿关节炎有治疗作用，可抑制TNF-α诱导的滑膜细胞激活，其作用机制可能与其抑制NLRP3/caspase-1信号通路有关。更多还原

【Abstract】 Objective To determine the effect of total saponins from Clematis henryi Oliv.(TsCH) on the activation of synovial cells and its possible mechanism. Methods In vitro experiment: synovial cells were pre-incubated with various concentrations of TsCH for 12 h, before being treated with tumor necrosis factor-α(TNF-α). After the treatment, CCK-8 and flow cytometry were used to detect the cell proliferation and cell cycle, respectively. Transwell detected the cell migration, and ELISA was used to detect the level of IL-18 and IL-1β. The expression of NLRP3, Caspase-1, MMP2 and MMP9 were detected by Western blot. Animal experiment: collagen-induced rat rheumatoid arthritis model was established. After 4 weeks of intragastric treatment with TsCH, the arthritis index score, paw volume and thickness were evaluated.The expression level of IL-1β, IL-18, NLRP3 and Caspase-1 in the rat joint tissue was detected. Results The in vitro experiment indicated that TsCH inhibited TNF-α-induced synovial cell proliferation and migration, and inhibited the expression level of IL-18, IL-1β, NLRP3, Caspase-1, MMP2 and MMP9. The animal experiments showed that TsCH decreased the arthritis index score, paw volume and thickness, and attenuated the level of TNF-α, IL-18, IL-1β, NLRP3 and Caspase-1 in the joint tissue. Conclusion Ts CH has therapeutic effect on rheumatoid arthritis and can inhibit TNF-α induced activation of synovial cells,whose mechanism may be related to its inhibition of the activation of NLRP3/Caspase-1 signaling pathway.更多还原