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目的:观察雷公藤多甙对IL-1β诱导大鼠滑膜细胞株RSC-364增殖和IL-6分泌的影响,探讨其治疗类风湿性关节炎的作用机理。方法:培养大鼠滑膜细胞株RSC-364,运用CCK-8法检测不同剂量的雷公藤多甙对IL-1β诱导大鼠滑膜细胞株RSC-364增殖的影响,酶联免疫吸附实验检测细胞株培养上清中的IL-6的含量。结果:经过IL-1β诱导大鼠滑膜细胞株RSC-364,在不同浓度的雷公藤多甙的作用48h后,其增殖明显受到抑制,并呈剂量依赖性。同时各剂量组均可抑制IL-1β诱导大鼠滑膜细胞株RSC-364分泌炎性因子IL-6的分泌。结论:雷公藤多甙抑制IL-1β诱导大鼠滑膜细胞株RSC-364的过度增殖和IL-6的分泌,这可能是其治疗类风湿性关节炎的作用机理之一。
OBJECTIVE: To observe the effects of Tripterygium wilfordii on the proliferation of IL-1β-induced rat synovial cell line RSC-364 and the secretion of IL-6, and to explore its mechanism of action in the treatment of rheumatoid arthritis. METHODS: Rat synoviocytes (RSC-364) were cultured and the effects of different doses of Tripterygium wilfordii on the proliferation of rat synovial cell line RSC-364 induced by IL-1β were detected by CCK-8 method. The results were detected by enzyme-linked immunosorbent assay. The content of IL-6 in the cell culture supernatant. RESULTS: After synovial cell line RSC-364 was induced by IL-1β, the proliferation of RSC-364 was inhibited at different concentrations of Tripterygium wilfordii for 48 h, and the proliferation was inhibited in a dose-dependent manner. At the same time, each dose group can inhibit IL-1β-induced secretion of inflammatory cytokines IL-6 secreted by rat synovial cell line RSC-364. Conclusion: Tripterygium wilfordii can inhibit IL-1β-induced hyperproliferation and secretion of IL-6 in rat synovial cell line RSC-364, which may be one of the mechanisms for the treatment of rheumatoid arthritis.