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机构地区:[1]广东医学院附属深圳南山医院中心实验室,深圳518052
出 处:《热带医学杂志》2008年第12期1220-1221,1224,共3页Journal of Tropical Medicine
基 金:深圳市科技和信息局项目(No.200405067)
摘 要:目的探讨雷公藤多甙(Tripterygium Glycosides,TG)对IL-1β诱导大鼠滑膜细胞株RSC-364JNK1的影响,进一步阐明雷公藤多甙治疗类风湿性关节炎的作用机制。方法运用Western-blot检测不同浓度的雷公藤多甙(0、5、10、20mg/L)对IL-1β诱导大鼠滑膜细胞株RSC-364JNK1蛋白的表达。结果雷公藤多甙明显地抑制IL-1β诱导大鼠滑膜细胞株RSC-364对JNK1蛋白的表达。结论雷公藤多甙抑制IL-1β诱导大鼠滑膜细胞株RSC-364对JNK1蛋白的表达,可能是其治疗类风湿性关节炎的重要作用机制之一。Objective To investigate the effect of Tripterygium Glycosides (TG) on e-Jun N-terminal kinase (JNK1) expression of rat synovial cell line RSC-364 stimulated with interleukin-1 beta(IL-1β) and to illuminate the mechanism of TG in the treatment of rheumatoid arthritis (RA). Method The expression of JNK1 of the rat synvoial cell line RSC-364 stimulated with IL-1β induced by different doses of TG(0, 5, 10, 20mg/L) were detected by Western-blot. Result The expression of JNK1 of the rat synvoial cell line RSC-364 stimulated with IL-1β induced by TG were obviously suppressed. Conclusion The expression of JNK in the rat synovial cell line RSC-364 stimulated with IL-1β was inhibited by TG, which might be the potential mechanism in the treatment of RA.
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