大鼠视前区巨噬细胞炎性蛋白-1β抗体未能抑制前列腺素E2引起的发热。

Antibodies to macrophage inflammatory protein-1beta in preoptic area of rats fail to suppress PGE2 hyperthermia.

作者信息

Armengol J A, Benamar K, Fernández-Alonso A, Sancibrián M, Myers R D, Miñano F J

机构信息

Departamento de Ciencias Morfologicas Facultad de Medicina, Universidad de Sevilla, Spain.

出版信息

Brain Res. 1997 Feb 14;748(1-2):245-9. doi: 10.1016/s0006-8993(96)01362-5.

DOI:10.1016/s0006-8993(96)01362-5

PMID:9067470

Abstract

This study determined whether macrophage inflammatory protein-1beta (MIP-1beta) plays a role in the hyperthermia caused by prostaglandin E2 (PGE2) given intracerebroventricularly (i.c.v.) in the rat. In these experiments, anti-murine MIP-1beta antibody (anti-MIP-1beta) was micro-injected in the anterior hypothalamic, preoptic area (AH/POA) just before i.c.v. PGE2. The results showed that anti-MIP-1beta failed to alter the PGE2 hyperthermia. However, immunocytochemical studies revealed MIP-1beta immunoreactivity detectable in both the organum vasculosum laminae terminalis (OVLT) and AH/POA in the febrile rat. These data thus demonstrate that MIP-1beta is sequestered in diencephalic structures underlying thermoregulation even though it is not involved in PGE2 hyperthermia. This dissociation supports the viewpoint that at least two distinct systems exist in the brain which underlie a febrile response: MIP-1beta underlies one component whereas PGE2 comprises the other.

摘要

本研究确定了巨噬细胞炎性蛋白-1β（MIP-1β）在大鼠脑室内注射前列腺素E2（PGE2）所致高热中是否起作用。在这些实验中，于脑室内注射PGE2之前，将抗小鼠MIP-1β抗体（抗MIP-1β）微量注射到下丘脑前部视前区（AH/POA）。结果显示，抗MIP-1β未能改变PGE2所致高热。然而，免疫细胞化学研究显示，在发热大鼠的终板血管器（OVLT）和AH/POA中均可检测到MIP-1β免疫反应性。因此，这些数据表明，尽管MIP-1β不参与PGE2所致高热，但它被隔离在体温调节的间脑结构中。这种分离支持了以下观点：大脑中至少存在两个不同的系统作为发热反应的基础，MIP-1β是其中一个组成部分的基础，而PGE2则构成另一个组成部分。