皮质酮和地塞米松在引起糖皮质激素受体下调方面的生物效能。

Biopotency of corticosterone and dexamethasone in causing glucocorticoid receptor downregulation.

作者信息

Svec F

出版信息

J Steroid Biochem. 1985 Nov;23(5A):669-71. doi: 10.1016/0022-4731(85)90020-2.

Abstract

The biopotencies of dexamethasone and corticosterone in causing glucocorticoid receptor downregulation in the AtT-20 cell were assessed and compared to their affinity for the isolated, cytosolic glucocorticoid receptor. Dexamethasone depleted receptor by 50% at a concentration of 4.6 nM. Its Kd for the receptor was 9.1 nM. The comparable values for corticosterone were 520 and 18.8 nM respectively. These results suggest that receptor depletion is a receptor mediated process; at some point the steroid must be bound to receptor in order to cause depletion. Further, the discrepancies between the two values for corticosterone support the hypothesis that it is the transformed receptor that is depleted.

摘要

评估了地塞米松和皮质酮在AtT - 20细胞中引起糖皮质激素受体下调的生物活性，并将其与它们对分离的胞质糖皮质激素受体的亲和力进行了比较。地塞米松在浓度为4.6 nM时使受体减少50%。其对受体的解离常数（Kd）为9.1 nM。皮质酮的相应值分别为520 nM和18.8 nM。这些结果表明受体减少是一个受体介导的过程；在某个时刻，类固醇必须与受体结合才能导致减少。此外，皮质酮的两个值之间的差异支持了被消耗的是转化受体这一假设。