Koike R, Miki I, Otoshi M, Totsuka T, Inoue H, Kase H, Saito I, Miyasaka N
First Department of Medicine, School of Medicine, Tokyo Medical and Dental Univeristy, Japan.
Mol Pharmacol. 1994 Oct;46(4):599-604.
We examined whether antirheumatic drugs alter cytokine- or lipopolysaccharide-induced expression of adhesion molecules on vascular endothelial cells. Human umbilical cord vein endothelial cells were co-cultured with various antirheumatic drugs in the presence of inflammatory cytokines, and adhesion molecule expression was measured by cell enzyme-linked immunosorbent assay and Northern blot analysis. Among these antirheumatic drugs, gold sodium thiomalate significantly inhibited intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression on vascular endothelial cells and suppressed cellular binding between human monocytic cell lines, including U937 and HL-60 cells, and interleukin-1 beta-stimulated vascular endothelial cells. It is speculated that down-regulation of adhesion molecules might be one of the novel mechanisms of action of gold sodium thiomalate.
我们研究了抗风湿药物是否会改变细胞因子或脂多糖诱导的血管内皮细胞上黏附分子的表达。在炎性细胞因子存在的情况下,将人脐静脉内皮细胞与各种抗风湿药物共同培养,并通过细胞酶联免疫吸附测定和Northern印迹分析来检测黏附分子的表达。在这些抗风湿药物中,硫代苹果酸金钠显著抑制血管内皮细胞上细胞间黏附分子-1和血管细胞黏附分子-1的表达,并抑制包括U937和HL-60细胞在内的人单核细胞系与白细胞介素-1β刺激的血管内皮细胞之间的细胞结合。据推测,黏附分子的下调可能是硫代苹果酸金钠作用的新机制之一。