特异性阿片受体μ、κ和δ拮抗剂在IL-1β所致体温升高中的作用

Effects of Selective μ,κ and δ Opioid Receptor Antagonist on Interleukin 1β Induced Hyperthermia

下丘脑视前区前部（ＰＯＡＨ）是经典的体温调控中枢，并存在有阿片受体。本研究旨在了解细胞介素ＩＬ－１β所致的体温升高是否与产生的内源性阿片有关，以及通过何种类型的阿片受体介导此升体温效应。研究使用雄性Ｓ－Ｄ大鼠，于自由状态下向其ＰＯＡＨ区微量注射ＩＬ－１β，注射前３０ｍｉｎ先向该区分别注射特异性阿片受体μ的拮抗剂ＣＴＡＰ，受体κ的拮抗剂ｎｏｒ－ＢＮＩ，受体δ的拮抗剂ＮＴＩ以及通常的阿片受体拮抗剂Ｎａｌ，用Ｓａｌ做对照。结果：ＩＬ－１β单独给药引起剂量相关的体温升高；经ＣＴＡＰ或者ＮＴＩ处理后，使ＩＬ－１β所致的体温升高作用减弱；Ｎａｌ能完全阻断ＩＬ－１β的升体温效应；而ｎｏｒ－ＢＮＩ对ＩＬ－１β的升体温效应无影响。

IL 1β is a cytokine present within the brain that produces marked hyperthermia when it is administered into the preoptic anterior hypothalamus (POAH), a primary central control site for body temperature (Tb) regulation. Opioid receptors exist in this region and hyperthermia can be elicited by μ selective opioid agonist injected there. This study was undertaken to investigate whether endogenous opioids are involved in the IL 1β induced hyperthermia and, if so, which type of opioid receptor mediates this effect. The selective μ opioid receptor antagonist CTAP, κ opioid receptor antagonist nor BNI, δ opioid receptor antagonist naltrindole (NTI) or the general opioid receptor antagonist naloxone (Nal) was microinjected into the POAH of unrestrained male S D rats 30 min before IL 1β microinjected into the same region. IL 1β alone caused a dose dependent hyperthermia. Hyperthermia caused by IL 1β was reduced by pretreatment with CTAP or NTI and completely blocked by pretreatment with Nal. Nor BNI did not affect IL 1β induced hyperthermia.