大鼠中前列腺素E2诱导的体温过高的EP1受体介导作用

EP1-receptor mediation of prostaglandin E2-induced hyperthermia in rats.

作者信息

Oka T, Hori T

机构信息

Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Am J Physiol. 1994 Jul;267(1 Pt 2):R289-94. doi: 10.1152/ajpregu.1994.267.1.R289.

DOI:10.1152/ajpregu.1994.267.1.R289

PMID:7914071

Abstract

To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E2 (PGE2), PGE2 and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (Tco) were observed in a 23 +/- 1 degrees C environment. 17-Phenyl-omega-trinor-PGE2 (an EP1 agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in Tco. Even though the EP1 agonist was 10 times less potent than PGE2 on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE2-induced one. No fever was elicited by an LCV injection of butaprost (an EP2 agonist; 0.1-100 nmol), 11-deoxy-PGE1 (an EP2 agonist; 0.1-1.0 nmol). The PGE2 (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP1 antagonist. The results suggest that the PGE2-induced hyperthermia in the rat is mediated predominantly through EP1 receptors in the brain.

摘要

为了研究何种前列腺素受体参与脑源性前列腺素E2（PGE2）诱导的发热过程，将PGE2及其类似物注入大鼠侧脑室（LCV），并在23±1℃环境下观察结肠温度（Tco）的变化。17-苯基-ω-三降-PGE2（一种EP1激动剂；0.01 - 10 nmol）可使Tco迅速且呈剂量依赖性升高。尽管按摩尔计算，EP1激动剂的效力比PGE2低10倍，但其热疗的时间进程与PGE2诱导的热疗非常相似。侧脑室注射布他前列素（一种EP2激动剂；0.1 - 100 nmol）、11-脱氧-PGE1（一种EP2激动剂；0.1 - 1.0 nmol）均未引起发热。用EP1拮抗剂SC-19220（150 nmol）对侧脑室进行预处理可阻断PGE2（0.3 nmol）诱导的热疗。结果表明，大鼠中PGE2诱导的热疗主要通过脑中的EP1受体介导。