Vanadium regulates HSP60-induced IL-6 release from RAW264.7 cells in a dose-dependent manner  

钒化合物调节RAW264.7细胞中热休克蛋白60诱导的IL-6释放(英文)

作　　者：郭巍[1,2] 杨晓达 

机构地区：[1]北京大学医学部药学院化学生物学系 [2]天然药物及仿生药物国家重点实验室,北京100191

出　　处：《Journal of Chinese Pharmaceutical Sciences》2015年第1期28-33,共6页中国药学（英文版）

基　　金：National Natural Science Foundation of China(Grant No.21271012)

摘　　要：Vanadium compounds are promising anti-diabetic agents. However, the underlying mechanisms have not been fully elucidated. Inflammation and auto-immune disorders play important roles in the progresses of both type Ⅰ and type Ⅱ diabetes, in which heat shock protein 60 （HSP60） is an important endogenous inflammatory mediator. In the present work, we investigated the effects of vanadium compounds （vanadyl sulfate and sodium metavanadate） on the IL-6 production in RAW264.7 cells upon HSP60 stimulation. Our data revealed that both vanadyl ions regulated the IL-6 expression in a concentration-dependent manner. However, the two common NF-κB and PPAR-γ, signal pathways were not involved in this process. Further works are needed to elucidate the underlying mechanism and significance of the immuno-modification actions for the pharmacological applications of anti-diabetic vanadium compounds.钒化合物是具有前景的抗糖尿病候选药物,但其药理作用机制尚未完全阐明。在I型和II型糖尿病发病过程中,炎症和自免疫紊乱可能发挥了重要作用?其中热休克蛋白60(HSP60)是关键的内源性促炎因子之一。本文研究了偏钒酸钠和硫酸氧钒两种化合物对R AW264.7巨噬细胞在HSP60刺激下分泌白细胞介素6(IL-6)的作用。结果表明,两种钒化合物均可浓度依赖的调节I L-6的表达。然而,钒化合物的作用并没有通过NF-κB和PPAR-γ这两种常见的炎症信号调节机制。本文结果提示,钒化合物调节免疫的作用可能与其抗糖尿病药理作用机制有关,值得深入的研究阐明。

关 键 词：Vanadyl ions Heat shock protein 60 INTERLEUKIN-6 

分 类 号：R96[医药卫生—药理学]