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内皮素受体参与大剂量细菌内毒素引起的发热反应。

ET receptors are involved in the febrile response induced by high dose of bacterial endotoxin.

机构信息

Department of Pharmacology, Federal University of Paraná, Centro Politécnico, PO Box 19031, Curitiba, PR, 81531-980, Brazil.

Department of Pharmacology, Federal University of Paraná, Centro Politécnico, PO Box 19031, Curitiba, PR, 81531-980, Brazil.

出版信息

J Therm Biol. 2021 Jan;95:102804. doi: 10.1016/j.jtherbio.2020.102804. Epub 2020 Dec 4.

DOI:10.1016/j.jtherbio.2020.102804
PMID:33454036
Abstract

Previous studies have demonstrated that endothelin-1 (ET-1) is involved in the febrile response induced by lipopolysaccharide (LPS) in male and female rats. This peptide induces fever acting on ET receptors in the central nervous system. However, during sepsis, endothelinergic ET receptors in the brain also exert an important role reducing the mortality of the animals. The present study evaluated the participation of ET receptors in the febrile response induced by different doses LPS in rats. Male Wistar rats were treated with the ET receptor antagonist BQ123 before or after the injection of a low dose (10 μg/kg) or a high dose (200 μg/kg) of LPS intraperitoneally. The febrile response was evaluated. The treatment with BQ123, in both protocols did not change the febrile response induced by the lower dose of LPS. The pre-treatment with BQ123 also did not significantly change the febrile response induced by a higher dose of LPS but the post-treatment with the antagonist abolished the febrile response induced by this dose of LPS. These results suggest that even though ET receptors are not recruited in the febrile response induced by lower doses of LPS, they are involved in the febrile response induced by high doses of this stimulus.

摘要

先前的研究表明,内皮素-1(ET-1)参与了脂多糖(LPS)诱导的雄性和雌性大鼠发热反应。这种肽通过作用于中枢神经系统中的 ET 受体引起发热。然而,在败血症期间,大脑中的内皮素能 ET 受体也发挥了重要作用,降低了动物的死亡率。本研究评估了 ET 受体在不同剂量 LPS 诱导的大鼠发热反应中的参与。雄性 Wistar 大鼠在腹腔内注射低剂量(10μg/kg)或高剂量(200μg/kg)LPS 之前或之后用 ET 受体拮抗剂 BQ123 处理。评估发热反应。在两种方案中,BQ123 的治疗均未改变低剂量 LPS 诱导的发热反应。BQ123 的预处理也未显著改变高剂量 LPS 诱导的发热反应,但拮抗剂的后处理消除了该剂量 LPS 诱导的发热反应。这些结果表明,即使 ET 受体未被募集到低剂量 LPS 诱导的发热反应中,它们也参与了高剂量 LPS 诱导的发热反应。

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