摘要
目的:探讨雷公藤甲素(TP)对肿瘤坏死因子(TNF-α)诱导的类风湿关节炎患者成纤维样滑膜细胞(RA-HFLS)增殖的影响及对Ras-MAPKs信号转导通路的调控作用。方法:不同浓度的TP(0.28,2.8,28,140 nmol.L-1)与RA-HFLS共孵育,采用MTS比色法检测细胞增殖活性,并通过Western blot检测不同浓度的TP对TNF-α诱导的RA-HFLS Ras-MAPKs信号转导通路相关蛋白(Ras,p-P38,p-ERK,p-JNK)表达水平的影响。结果:MTS结果显示,TP可以剂量依赖性抑制RA-HFLS的增殖,其抑制率分别为0.28%,5.05%,30.83%,43.77%;Western blot结果提示TP可剂量依赖性抑制Ras-MAPKs信号转导通路相关蛋白的表达。结论:TP能抑制RA-HFLS增殖、减轻滑膜炎症,其分子机制可能与调控了Ras-MAPKs信号转导通路的异常活化有关。
Objective： To investigate the effects of triptolide on proliferation and regulation of Ras-MAPKs pathway in human fibroblast-like synoviocytes of Rheumatoid Arthritis（RA-HFLS） treated with tumor necrosis factor （TNF-α）. Methods： RA-HFLS were cultured with TNF-α in the presence or absence of variable doses of triptolide （0.28, 2.8, 28, 140 nmol？L-1） in vitro. Cell proliferation was evaluated by MTS assay. The phosphorylation status of Ras-MAPKs-associated proteins （Ras,p-P38,p-ERK and p-JNK） were detected by Western blot analysis. Results： Triptolide could obviously decrease the RA-HFLS viability in a dose-dependent style and the inhibition ratio were 0.28%, 5.05%, 30.83% and 43.77% respectively. In addition, triptolide could also suppressed the expression of Ras, p-P38, p-ERK and p-JNK. Conclusion： Triptolide has an notable inhibiting effect on proliferation of RA-HFLS and the molecule mechanism is due in part to the direct suppression of abnormal activation of Ras-MAPKs pathway.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2010年第7期888-891,共4页
China Journal of Chinese Materia Medica
基金
北京市自然科学基金项目(7062051)
关键词
类风湿关节炎
成纤维样滑膜细胞
雷公藤甲素
MAPKS
Rheumatoid arthritis human fibroblast-like synoviocytes of Rheumatoid Arthritis triptolide MAPKs
