目的：观察穿山龙水溶性总皂苷对TNF-α加IL-17诱导的大鼠成纤维样滑膜细胞株RSC-364核转录因子NF-κB活化的调控作用及下游基因TNF-α、IL-1、ICAM-1、MMP-2、MMP-3分泌的影响。方法: 用IL-17加TNF-α刺激RSC-364建立类风湿性关节炎（RA）细胞模型，以不同浓度穿山龙水溶性总皂苷干预，采用半定量RT-PCR的方法检测各组NF-κBp65 基因和IκB-α基因的表达，酶联免疫吸附试验（ELISA）检测细胞培养液上清中TNF-α、IL-1、ICAM-1、MMP-2、MMP-3蛋白水平的变化。结果：穿山龙水溶性总皂苷可呈浓度依赖性抑制TNF-α加IL-17刺激的RSC-364中NF-κBp65的活化，提升IκB-α的表达，并抑制TNF-α、IL-1、ICAM-1、MMP-2、MMP-3的分泌。结论：穿山龙水溶性总皂苷可抑制NF-κB通路的活化，阻碍下游多种基因的分泌与活化，提示其可能具有抑制RA滑膜炎症的作用。

This study was aimed to observe the influence of water-solubility nipponica saponin on activation of TNF-α+IL-17-induced rat fibroblast-like synovial cell line RSC-364 cellular model nuclear transcription factor NF-κB pathway as well as TNF-α, IL-1, ICAM-1, MMP-2, MMP-3 secretion. IL-17+ TNF-琢were used for stimulating RSC-364 to establish rheumatoid arthritis (RA) cellular model. Water-solubility nipponica saponin in different concentrations was used for intervention. The influence of water-solubility nipponica saponin in different concentrations on cell viability was detected by semi-quantitative RT-PCR method. Changes in the level of TNF-α, IL-1, ICAM-1, MMP-2, and MMP-3 of culture supernatant were detected by ELISA. The results showed that the activation of NF-κB p65 in RSC-364 stimulated by TNF-α+ IL-17 can be inhibited by water-solubility nipponica saponin according to its concentration. It improved IκB-α expression, and inhibited TNF-α, IL-1, ICAM-1, MMP-2 and MMP-3 secretion. It was concluded that water-solubility nipponica saponin can inhibit the activation of NF-κB pathway, hinder the secretion and activation of multiple downstream genes, which may be its effect in inhibiting synovial inflammation in RA.

河北省教育厅指令课题（2011163）：薯蓣皂苷对IL-17和TNF-α诱导大鼠滑膜细胞株NF-资B 通路的影响，负责人：段一娜；承德市科技局指导课题（201121024）：薯蓣皂苷片对类风湿关节炎的应用研究，负责人：段一娜；河北省教育厅高等学校科学技术项目（ZH200806）：穿山龙总皂苷对CIA大鼠化膜细胞炎性因子网络及NF-κB活性调控机制的研究，负责人：宋鸿儒；国家自然科学基金委重点项目（30873420）：穿山龙总皂苷对CIA大鼠血管新生相关细胞因子的影响及其调控机制的研究，负责人：宋鸿儒。