Marone G, Fimiani B, Petracca R, Marchese E, Condorelli M
Ric Clin Lab. 1985 Jan-Mar;15(1):25-32. doi: 10.1007/BF03029158.
Prolonged incubation (18h) of human polymorphonuclear leukocytes (PMNs) with betamethasone (BT) (10(-7) M) increased (3H)-DHA binding to human PMN membranes, apparently causing an increase in the number of beta-adrenergic receptors. Inhibition of this effect by cycloheximide (2 micrograms/ml) suggests that it is dependent on protein synthesis. BT had no effect on basal levels of cAMP in PMNs, but synergistically potentiated the increase in cyclic AMP (cAMP) induced by isoproterenol. Propranolol completely abolished the synergistic effect of BT plus isoproterenol, suggesting that the potentiating effect of BT on cAMP metabolism required the activation of beta-adrenergic receptors. Thus, BT increased the number of beta-adrenergic receptors in human PMN membranes and potentiated the cAMP changes induced by beta-agonists.
将人多形核白细胞（PMN）与倍他米松（BT）（10⁻⁷M）长时间孵育（18小时）会增加（³H）-DHA与人PMN膜的结合，这显然导致β-肾上腺素能受体数量增加。环己酰亚胺（2微克/毫升）对这种效应的抑制表明它依赖于蛋白质合成。BT对PMN中cAMP的基础水平没有影响，但协同增强了异丙肾上腺素诱导的环磷酸腺苷（cAMP）增加。普萘洛尔完全消除了BT加异丙肾上腺素的协同效应，这表明BT对cAMP代谢的增强作用需要β-肾上腺素能受体的激活。因此，BT增加了人PMN膜中β-肾上腺素能受体的数量，并增强了β-激动剂诱导的cAMP变化。
