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β-肾上腺素能受体在体内介导肾上腺素对脂多糖诱导的肿瘤坏死因子释放的抑制作用。

Beta-adrenergic receptors mediate in vivo the adrenaline inhibition of lipopolysaccharide-induced tumor necrosis factor release.

作者信息

Monastra G, Secchi E F

机构信息

Department of Immunology, Fidia Research Laboratories, Abano Terme, Italy.

出版信息

Immunol Lett. 1993 Oct;38(2):127-30. doi: 10.1016/0165-2478(93)90177-4.

Abstract

Adrenaline has been shown to inhibit the release of tumor necrosis factor (TNF) elicited by lipopolysaccharide (LPS) when tested in vitro on cultured human blood cells and rat macrophages. In this report we have examined the effect of the in vivo administration of adrenaline on TNF serum levels induced by LPS. In agreement with in vitro data, adrenaline (0.1 mg/kg, s.c.) was found to inhibit in the mouse the LPS-induced TNF release. The beta-adrenergic antagonist propranolol administered 1 h before adrenaline completely blocked the adrenaline activity, whereas the alpha-adrenergic antagonist phentolamine was ineffective. These data demonstrate that: (i) adrenaline is an effective antagonist of LPS-induced TNF release in vivo, and (ii) its effect is mediated by beta-adrenergic receptors.

摘要

在体外对培养的人血细胞和大鼠巨噬细胞进行测试时,已表明肾上腺素可抑制脂多糖(LPS)引发的肿瘤坏死因子(TNF)释放。在本报告中,我们研究了体内给予肾上腺素对LPS诱导的TNF血清水平的影响。与体外数据一致,发现肾上腺素(0.1mg/kg,皮下注射)可在小鼠中抑制LPS诱导的TNF释放。在肾上腺素给药前1小时给予的β-肾上腺素能拮抗剂普萘洛尔完全阻断了肾上腺素的活性,而α-肾上腺素能拮抗剂酚妥拉明则无效。这些数据表明:(i)肾上腺素是体内LPS诱导的TNF释放的有效拮抗剂,以及(ii)其作用是由β-肾上腺素能受体介导的。

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