致死性和非致死性烫伤大鼠胞液和胞核糖皮质激素受体的研究

本文以[~3H]地塞米松(Dex)为配体,用放射配体结合测定法研究了致死性和非致死性烫伤大鼠的肝、脑胞液中糖皮质激素受体(GCR)的变化,与对照组比较,两组烫伤大鼠肝、脑胞液的[~3H]Dex特异结合的结合容量(R_o)均减少,表观上的平衡解离常数(K_d)均增加;和非致死性烫伤组比较,致死性烫伤组R_o的减少更为明显。为了探讨胞液GCR的减少是否由于[~3H]Dex-GCR复合物转位到核内,用交换法测定了肝核的[~3H]B特异结合,结果对照组和烫伤组之间无明显差别。对这些变化的可能的机制和临床意义作了讨论。     

糖皮质激素对糖皮质激素受体的调节——Ⅱ.大鼠肝、脑、脾的研究

将氢化可的松(F)混合在聚乙烯醇(PVA)内,给大鼠皮下注射,将血浆糖皮质激素(GC)维持在应激浓度,20—40μg/dl 3天,结果发现肝胞液糖皮质激素受体(GR)的结合容量(R_0)和脾细胞GR的结合量(R_s)于注射后1h已明显减少,并维持于低水平。注射后7天,血浆GC已下降到正常水平,但GR恢复得较慢,直到11天脾细胞GR尚未完全恢复。GR的Kd不变,脑胞液GR的变化不明显。实验结果表明,在整体动物GC对GR和在培养细胞一样也存在着负调节,但对不同的靶器官,GR的负调节可能具有不同的特点。     

REGULATION OF GLUCOCORTICOID RECEPTOR BY GLUCOCORTICOIDS(Ⅱ) ——THE STUDIES ON RAT LIVER, BRAIN AND SPLEEN

The concentration of glucocorticoids (GC) in plasma was maintained at stress level, 20--40μg/dl, for 3 days by subcutaneous injection of hydrocortisone (F) in polyvinyl alcohol (PVA) into rats, and the specific binding of [~3H]Dexamethasone (Dex) in liver, spleen and brain was determined before and after injection. The binding capacity of glucocorticoid receptor (GR) in liver and spleen was decreased significantly 1 h after injection and maintained at low level for several days after the concentration of GC in plasma had returned to the normal level. The K_d was not altered. The changes of GR in brain was not significant. Thus it may be concluded that GC can down-regulate GR in rats, but with different characteristics in various target organs.     

A STUDY OF THE GLUCOCORTICOID RECEPTOR OF THE CYTOSOL AND NUCLEI IN NONLETHALLY AND LETHALLY SCALDED RATS

The glucocorticoid receptor (GCR) of the cytosol of liver and brain was studied by radioligand binding assay, using [~3H] dexamethasone (Dex) as the ligand in lethally and nonlethally scalded rats. As compared with controls, the binding capacity (R_0) was decreased and the apparent K_d of [~3H] Dex specific binding was increased in both scalded groups. In the lethal group, the R_u is much lower than that in the nonlethal group. In order to determine whether the decrease of R_0 was due to the translocation of [~3H] Dex-GCR complex into the cell nuclei, the [~3H] corticosterone (B) specific binding of the hepatic nuclei was measured by the exchange assay. There was no significant difference between the control and scalded groups. The possible mechanisms and the clinical significance of these changes were discussed.