Falus A, Biró J, Rákász E
Department of Biology, Semmelweis Medical University, Budapest, Hungary.
Ann N Y Acad Sci. 1995 Jul 21;762:71-7; discussion 77-8. doi: 10.1111/j.1749-6632.1995.tb32315.x.
The role of the inflammatory cytokines on glucocorticosteroid binding (GCSB) and glucocorticosteroid receptor (GR) level was studied. We incubated a B cell line--CESS--, a promonocytic cell line--U937--and a hepatoma cell line--HepG2--in the presence of varying concentrations of IL-1 beta, IL-6 and TNF-alpha for 24 hours. Glucocorticosteroid binding was determined by the method of "whole cell uptake," and characterized by Scatchard analysis. A considerable increase in the glucocorticosteroid binding was induced by all the three cytokines. Northern analysis of the glucocorticoid receptor expression demonstrates that the action of the cytokines is likely not pretranslational. Present data suggest that local imbalance in the ratio of these three cytokines in different pathological cases might influence the glucocorticosteroid sensitivity of the lymphocytes, monocytes and hepatocytes as target cells.
研究了炎性细胞因子对糖皮质激素结合（GCSB）及糖皮质激素受体（GR）水平的作用。我们在不同浓度的白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）存在的情况下，将一种B细胞系——CESS、一种原单核细胞系——U937和一种肝癌细胞系——HepG2孵育24小时。糖皮质激素结合通过“全细胞摄取”法测定，并通过Scatchard分析进行表征。所有这三种细胞因子均诱导糖皮质激素结合显著增加。糖皮质激素受体表达的Northern分析表明，细胞因子的作用可能不是翻译前的。目前的数据表明，在不同病理情况下这三种细胞因子比例的局部失衡可能会影响作为靶细胞的淋巴细胞、单核细胞和肝细胞的糖皮质激素敏感性。
