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参与聚肌苷酸-聚胞苷酸诱导的发热反应的中枢介质:内皮素和P物质未参与其中。

Central mediators involved in the febrile response induced by polyinosinic-polycytidylic acid: lack of involvement of endothelins and substance P.

作者信息

Bastos-Pereira A L, Leite M C G, Fraga D, Zampronio A R

机构信息

Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil.

Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil.

出版信息

J Neuroimmunol. 2015 Jan 15;278:100-7. doi: 10.1016/j.jneuroim.2014.12.011. Epub 2014 Dec 13.

DOI:10.1016/j.jneuroim.2014.12.011
PMID:25595258
Abstract

The present study evaluated the involvement of interleukin(IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, interferon(IFN)-γ, prostaglandins of the E2 series, endothelins, substance P and opioids within the central nervous system in polyinosinic:polycytidylic acid (Poly I:C)-induced fever in rats. Poly I:C injection induced a febrile response which was reduced by intracerebroventricular administration of the antibodies against TNF-α, IL-6, or IFN-γ, or by IL-1 or μ receptor antagonists. Intraperitoneal injection of indomethacin or oral administration of celecoxib also reduced Poly I:C-induced fever. Poly I:C increased prostaglandin E2 levels in the cerebrospinal fluid of the animals which was also reduced by indomethacin. The intracerebroventricular injection of ETB or NK1 receptor antagonists did not alter Poly I:C-induced fever. These data suggest the involvement of IL-1β, TNF-α, IL-6, IFN-γ, prostaglandin E2, and opioids but not endothelins and substance P on Poly I:C-induced fever.

摘要

本研究评估了白细胞介素(IL)-1β、肿瘤坏死因子-α(TNF-α)、IL-6、干扰素(IFN)-γ、E2系列前列腺素、内皮素、P物质和阿片类物质在聚肌苷酸:聚胞苷酸(Poly I:C)诱导的大鼠中枢神经系统发热中的作用。注射Poly I:C可引起发热反应,脑室内注射抗TNF-α、IL-6或IFN-γ抗体,或注射IL-1或μ受体拮抗剂可减轻该反应。腹腔注射吲哚美辛或口服塞来昔布也可减轻Poly I:C诱导的发热。Poly I:C可使动物脑脊液中前列腺素E2水平升高,吲哚美辛也可使其降低。脑室内注射ETB或NK1受体拮抗剂不会改变Poly I:C诱导的发热。这些数据表明,IL-1β、TNF-α、IL-6、IFN-γ、前列腺素E2和阿片类物质参与了Poly I:C诱导的发热,而内皮素和P物质未参与。

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