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“阳虚”动物模型肝胞液糖皮质激素受体改变及助阳药的作用
引用本文:张家庆,谭金兴,刘振全. “阳虚”动物模型肝胞液糖皮质激素受体改变及助阳药的作用[J]. 中国中西医结合杂志, 1984, 0(2): 107-108,69
作者姓名:张家庆  谭金兴  刘振全
作者单位:第二军医大学长海医院内科,第二军医大学病理生理学教研室,第二军医大学长海医院内科
摘    要:本文以[~3H]地塞米松为配体,用交换法测定糖皮质激素受体(GCR)的结合容量(Ro)及解离常数(Kd)。以氢化考的松造成大鼠"阳虚"模型后,在末次注射后5或24小时处死者,肝胞液中 GCR 的 Ro 均明显减少,Kd 明显增大。但末次注射后48小时处死者已近于恢复。助阳药对此种 GCR 改变无影响。

关 键 词:动物模型  糖皮质激素受体  助阳药  氢化考的松  阳虚  解离常数  胞液  肾上腺皮质功能低下  皮质醇  地塞米松

Changes in Glucocorticoid Receptor of Liver Cytosol in "Yang Deficiency" Animal Models and Effects of "Yang-Tonifiers"
Zhang Jiaqing. Changes in Glucocorticoid Receptor of Liver Cytosol in "Yang Deficiency" Animal Models and Effects of "Yang-Tonifiers"[J]. Chinese journal of integrated traditional and Western medicine, 1984, 0(2): 107-108,69
Authors:Zhang Jiaqing
Abstract:The binding capacity(Ro)and the apparant dissociation constant(Kd)of glucocorticoid receptor(GCR)of liver cytosol in"Yang deficiency"animal models were estimated by way of exchange assay,using ~3H dexamethasone as the ligand.The levels of Ro from control groups were about 270 fmol/mg protein,and Kd were about 0.40.But the levels of Ro of"Yang deficiency"animals,which were produced by chronic injections of hydrocortisone for 20 days, were significantly decreased.The value of rats decapitated in 5 hours after the last injection of hydrocortisone was 155.5,and that in 24 hours was 174.0.Kd was markedly elevated,the figures being 1.43 and 1.66 respectively.There were statistically significant differences between the"Yang deficiency"groups and the control.The Ro and Kd of"Yang deficiency"rats decapitated in 48 hours after the last injection,however,almost returned to normal values. The addition of 4"Yang-tonifiers(prepared aconite root,cinnamon bark,epimedium and cistanche)had no effect on the Ro and Kd of GCR of"Yang deficiency"animals,suggesting that the 4"Yang-tonifiers"were of little avail with respect to the decrease in GCR. In general,the GCR level of the animal model is low,and there is an increase in Kd.This suggests that there may be some variation in the molecular structure of GCR.As for the cause of the decrease in GCR,the authors suggest that this may be due to the lowered synthesis rate of GCR as well as the influence of"down regulation"of glucocorticoids.
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