皮质类固醇抑制炎症介质的产生是一个糖皮质激素受体介导的过程。
Inhibition of the production of mediators of inflammation by corticosteroids is a glucocorticoid receptor-mediated process.
机构信息
Department of Pharmacology Faculty of Medicine and Health Sciences Erasmus University Rotterdam The Netherlands.
出版信息
Mediators Inflamm. 1996;5(2):100-3. doi: 10.1155/S0962935196000166.
In order to find an explanation for corticosteroid resistance we assessed whether inhibition by dexamethasone (DEX) of the stimulated production of TNF- proportional, variant, IL-6, PGE(2) and LTB(4) by peripheral blood mononuclear cells (MNC) depends on binding to the glucocorticoid receptor (GR), and whether it is determined by the number or the affinity of the GR of these cells. GR number and affinity of MNC were determined by means of a whole cell DEX binding assay. MNC were incubated with DEX and LPS or A23187 in the absence or presence of RU486, a potent steroid antagonist. DEX caused a concentration dependent inhibition of TNF- proportional, variant, IL-6 and PGE(2) production but had no effect on LTB(4) production. RU486 significantly blocked the effect of DEX, but no correlations were found between the inhibition of mediator release and the K(d) or receptor number.
为了寻找皮质类固醇抵抗的解释，我们评估了地塞米松（DEX）是否通过外周血单核细胞（MNC）抑制刺激产生的 TNF-比例、变体、IL-6、PGE（2）和 LTB（4）取决于与糖皮质激素受体（GR）的结合，以及它是否取决于这些细胞的 GR 的数量或亲和力。通过全细胞 DEX 结合测定来确定 MNC 的 GR 数量和亲和力。在不存在或存在 RU486（一种有效的甾体拮抗剂）的情况下，将 MNC 与 DEX 和 LPS 或 A23187 孵育。DEX 浓度依赖性地抑制 TNF-比例、变体、IL-6 和 PGE（2）的产生，但对 LTB（4）的产生没有影响。RU486 显著阻断了 DEX 的作用，但在介质释放的抑制与 K（d）或受体数量之间未发现相关性。
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