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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 drug candidates, but their pharmacological mechanisms have not yet been fully elucidated. In the pathogenesis of type I and type II diabetes, inflammation and immune disorders may play an important role in which heat shock protein 60 (HSP60) is one of the key endogenous proinflammatory cytokines. In this paper, the effects of sodium metavanadate and vanadyl sulfate on the secretion of interleukin-6 (IL-6) stimulated by HSP60 in R AW264.7 macrophages were studied. The results showed that both vanadium compounds can regulate the expression of IL-6 in a concentration-dependent manner. However, the vanadium compounds did not pass the two common inflammatory signaling mechanisms NF-κB and PPAR-γ. Our results suggest that vanadium compounds regulate immune function may be related to its anti-diabetic pharmacological mechanism, it is worth further study to clarify.