Lundgren J D, Hirata F, Marom Z, Logun C, Steel L, Kaliner M, Shelhamer J
Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892.
Am Rev Respir Dis. 1988 Feb;137(2):353-7. doi: 10.1164/ajrccm/137.2.353.
The effect of glucocorticoids on respiratory glycoconjugate (RGC) secretion was studied in a cat tracheal organ culture system. Dexamethasone (10(-5) to 10(-9) M) added to culture medium for 24 h caused a dose-related reversible inhibition of RCG of as much as 40% with a peak effect at 24 to 60 h after initiation of dexamethasone treatment. A monoclonal antilipocortin antibody added to the cultures blocked the inhibitory effect of dexamethasone on RGC secretion and accelerated the reversal of the dexamethasone effect after discontinuation of dexamethasone treatment. A control antibody without antilipocortin activity had no effect on RGC secretion or dexamethasone-induced inhibition of RGC secretion. Measurement of the concentration of lipocortin in airways revealed a 220% increase after treatment with dexamethasone for 24 h. We conclude that dexamethasone inhibits RGC secretion through the induction of lipocortin synthesis.
在猫气管器官培养系统中研究了糖皮质激素对呼吸道糖缀合物(RGC)分泌的影响。将地塞米松(10^(-5)至10^(-9)M)添加到培养基中24小时,导致RGC出现剂量相关的可逆性抑制,抑制率高达40%,在地塞米松处理开始后24至60小时达到峰值效应。添加到培养物中的单克隆抗脂皮质素抗体可阻断地塞米松对RGC分泌的抑制作用,并加速地塞米松处理停止后地塞米松效应的逆转。无抗脂皮质素活性的对照抗体对RGC分泌或地塞米松诱导的RGC分泌抑制无影响。气道中脂皮质素浓度的测量显示,地塞米松处理24小时后增加了220%。我们得出结论,地塞米松通过诱导脂皮质素合成来抑制RGC分泌。