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白细胞介素-1(IL-1)对来自体外灌流大鼠下丘脑-神经垂体复合体的大鼠促肾上腺皮质激素释放因子(CRF)释放的刺激作用,该作用独立于胆碱能机制。

Stimulation by interleukin-1 (IL-1) of the release of rat corticotropin-releasing factor (CRF), which is independent of the cholinergic mechanism, from superfused rat hypothalamo-neurohypophysial complexes.

作者信息

Ohgo S, Nakatsuru K, Oki Y, Ishikawa E, Matsukura S

机构信息

Department of Medicine, Miyazaki Medical College, Japan.

出版信息

Brain Res. 1991 Jun 7;550(2):213-9. doi: 10.1016/0006-8993(91)91320-z.

DOI:10.1016/0006-8993(91)91320-z
PMID:1679371
Abstract

The effects of interleukin-1 (IL-1) and interferon-gamma (Ifn-gamma) on the release of corticotropin-releasing factor (CRF) from superfused hypothalamo-neurohypophysial complexes (HNC) of rats were examined in the present study. In this in vitro system, the release of CRF from HNC was not affected by any dose of human recombinant Ifn-gamma tested (0.1, 1 and 10 nM). In contrast, a rapid increase of CRF from HNC was elicited in a dose-dependent manner by human recombinant IL-1 alpha and -1 beta in concentrations of 0.1-10 nM. The involvement of the cholinergic system in the mediation of the stimulatory effect of IL-1 on CRF release was evaluated. Acetylcholine in concentrations of 1-100 nM also elicited a rapid increase of CRF. The increase in CRF release induced by 10 nM of acetylcholine was completely suppressed in the presence of both hexamethonium (10 microM) and atropine (50 microM), a nicotinic and a muscarinic receptor antagonist, respectively. On the other hand, the increase in CRF release induced by 10 nM IL-1 alpha or -1 beta was not affected by these two antagonists. These results indicate that IL-1 stimulates CRF release through an action on the hypothalamo-neurohypophysial system, most likely on the hypothalamus, and that the stimulatory effect of IL-1 is probably independent of the cholinergic system.

摘要

本研究检测了白细胞介素 -1(IL -1)和干扰素 -γ(Ifn -γ)对大鼠下丘脑 - 神经垂体复合体(HNC)超灌流时促肾上腺皮质激素释放因子(CRF)释放的影响。在这个体外系统中,所检测的任何剂量的人重组Ifn -γ(0.1、1和10 nM)均不影响HNC中CRF的释放。相反,浓度为0.1 - 10 nM的人重组IL -1α和 -1β以剂量依赖方式引起HNC中CRF迅速增加。评估了胆碱能系统在介导IL -1对CRF释放的刺激作用中的参与情况。浓度为1 - 100 nM的乙酰胆碱也引起CRF迅速增加。在分别存在烟碱受体拮抗剂六甲铵(10 μM)和毒蕈碱受体拮抗剂阿托品(50 μM)的情况下,10 nM乙酰胆碱诱导的CRF释放增加被完全抑制。另一方面,10 nM IL -1α或 -1β诱导的CRF释放增加不受这两种拮抗剂影响。这些结果表明,IL -1通过作用于下丘脑 - 神经垂体系统,很可能是下丘脑,刺激CRF释放,并且IL -1的刺激作用可能独立于胆碱能系统。

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