摘要
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 explore the treatment mechanism of Tripterygium Glycosides for rheumatoid arthritis with investigating the effect of Tripterygium Glycosides (TG) on the proliferation and secretion of interleukin -6 (IL -6 ) of rat synovial cell line 364 (RSC -364) cultures induced with interleukin - 1 beta (IL - 1 β). Methods TG (0, 5, 10, 20mg/L) solutions were added into RSC - 364 cultures, the proliferation of RSC - 364 induced with IL - 1 β at different strength of TG was detected with cell counting Kit - 8 ( CCK - 8 ) assay and the expression of IL - 6 in the supernatant was detected with enzyme - linked immunosorbent assays. Resuits The proliferation and the secretion of IL - 6 of RSC - 364 induced with IL - 1 β were significantly inhibited with the addition of different strength of TG and the inhibition was dose - dependent. Gonclusion The proliferation and the secretion of IL - 6 of RSC - 364 induced with IL - 1 β were suppressed by TG, which was possibly related to the mechanism of treatment of RA.
出处
《放射免疫学杂志》
CAS
2007年第6期546-547,共2页
Journal of Radioimmanology