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环已酰亚胺可抑制甲状腺功能减退大鼠垂体 T3 核受体受 3,5,3'-三碘甲状腺原氨酸(T3)的调节作用。

The modulation by 3,5,3'-triiodothyronine (T3) of pituitary T3 nuclear receptors in hypothyroid rats is inhibited by cycloheximide.

作者信息

Lemarchand-Béraud T, Von Overbeck K, Rognoni J B

出版信息

Endocrinology. 1987 Aug;121(2):677-83. doi: 10.1210/endo-121-2-677.

DOI:10.1210/endo-121-2-677
PMID:3595537
Abstract

The density of T3 nuclear receptors is known to vary with tissues and physiopathological conditions, but the factors involved in their regulation are still unknown. We have previously shown in the anterior pituitary gland that T3 modulates its own receptors; the density of T3 receptors in hypothyroid rats is half that in normal rats, and one injection of T3 is able to restore normal density of T3 receptors within 1-3 h. To determine whether T3 has a direct action on the synthesis of its nuclear receptor, the effect of cycloheximide (Cy) on T3-induced nuclear receptor was studied. In addition, the relationship between the density of pituitary T3 receptors and the secretion of TSH in different thyroid states was examined. In normal rats one injection of Cy (0.5-8 mg/100 mg BW) induced within 3 h a dose-dependent reduction in the density of pituitary T3 receptors as well as an important decrease in plasma TSH, with no changes in T4, T3, or pituitary TSH content. In hypothyroid rats the 50% decrease in the density of pituitary T3 receptors was not further reduced by 1 mg Cy. However, when the same dose of Cy was given 30 min before T3 it completely inhibited the induction by T3 of its receptors. When Cy was given 30 min or 1 h after T3 the inhibition was only partial. An inverse correlation was found between the density of T3 receptors in the pituitary gland and plasma TSH (r = -0.8128) in all experimental groups except those treated with Cy; this drug had an inhibitory effect on both TSH secretion and the density of receptors. The present data, therefore, support the view that T3 in the pituitary gland may induce the synthesis of its own nuclear receptors and that the density of T3 receptors is also involved in the control of TSH secretion.

摘要

已知T3核受体的密度会因组织和生理病理状况而有所不同,但其调控所涉及的因素仍不清楚。我们之前在前脑垂体中发现,T3可调节其自身的受体;甲状腺功能减退大鼠体内T3受体的密度是正常大鼠的一半,注射一次T3能够在1 - 3小时内使T3受体的密度恢复正常。为了确定T3对其核受体的合成是否具有直接作用,我们研究了环己酰亚胺(Cy)对T3诱导的核受体的影响。此外,还检测了不同甲状腺状态下垂体T3受体密度与促甲状腺激素(TSH)分泌之间的关系。在正常大鼠中,注射一次Cy(0.5 - 8毫克/100毫克体重)在3小时内会导致垂体T3受体密度呈剂量依赖性降低,同时血浆TSH显著减少,而T4、T3或垂体TSH含量没有变化。在甲状腺功能减退的大鼠中,1毫克Cy并未进一步降低垂体T3受体密度50%的降幅。然而,当在T3给药前30分钟给予相同剂量的Cy时,它会完全抑制T3对其受体的诱导作用。当在T3给药后30分钟或1小时给予Cy时,抑制作用只是部分的。在所有未用Cy处理的实验组中,垂体中T3受体的密度与血浆TSH之间呈负相关(r = -0.8128);这种药物对TSH分泌和受体密度均有抑制作用。因此,目前的数据支持这样一种观点,即垂体中的T3可能诱导其自身核受体的合成,并且T3受体的密度也参与了TSH分泌的调控。

相似文献

1
The modulation by 3,5,3'-triiodothyronine (T3) of pituitary T3 nuclear receptors in hypothyroid rats is inhibited by cycloheximide.环已酰亚胺可抑制甲状腺功能减退大鼠垂体 T3 核受体受 3,5,3'-三碘甲状腺原氨酸(T3)的调节作用。
Endocrinology. 1987 Aug;121(2):677-83. doi: 10.1210/endo-121-2-677.
2
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