Norton J M, Munck A
J Immunol. 1980 Jul;125(1):259-66.
In vitro exposure of homogeneous monolayer cultures of thioglycollate-elicited mouse peritoneal macrophages to glucocorticoid hormones for up to 96 hr produced a progressive, dose-related inhibition of cell growth and protein synthesis. The reductions in cell protein, incorporation of radiolabeled leucine, and intracellular water space were specific to steroids with glucocorticoid action, with half-maximal inhibition occurring at about 10(-9) M for dexamethasone. Similar dose-related, glucocorticoid-specific decreases in net glucose uptake, lactate production, and 14CO2 production were observed that were only partially explained by the decrease in cell mass. A decrease in the monosaccharide transport system Vmax was also noted but could be completely accounted for by the reduction in cell surface area and the resulting proportional loss in transport sites. No effect on transport system affinity could be demonstrated. The suggestion was made that such long-term culture of macrophages in the presence of glucocorticoids reverses the biochemical and functional changes that comprise the "activated" state of mononuclear phagocytes.
将巯基乙酸盐诱导的小鼠腹腔巨噬细胞的均匀单层培养物在体外暴露于糖皮质激素长达96小时,会产生细胞生长和蛋白质合成的渐进性、剂量相关抑制。细胞蛋白质、放射性标记亮氨酸掺入量和细胞内水空间的减少是具有糖皮质激素作用的类固醇所特有的,地塞米松的半数最大抑制浓度约为10^(-9) M。观察到净葡萄糖摄取、乳酸生成和14CO2生成也有类似的剂量相关、糖皮质激素特异性降低,这仅部分由细胞质量的减少来解释。还注意到单糖转运系统的Vmax降低,但这完全可以由细胞表面积的减少以及由此导致的转运位点比例性损失来解释。未证明对转运系统亲和力有影响。有人提出,在糖皮质激素存在下对巨噬细胞进行如此长期的培养会逆转构成单核吞噬细胞“活化”状态的生化和功能变化。