摘要
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。
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.
基金
National Natural Science Foundation of China(Grant No.21271012)
