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κ-阿片受体通过强啡肽对真鲷先天免疫反应的调节作用。

Kappa-opioid receptor-mediated modulation of innate immune response by dynorphin in teleost Channa punctatus.

机构信息

Department of Zoology, University of Delhi, Chattra Marg, North Campus, Delhi 110007, India.

出版信息

Peptides. 2010 May;31(5):973-8. doi: 10.1016/j.peptides.2010.01.009. Epub 2010 Feb 2.

Abstract

The immunomodulatory role of endogenous opioid peptides released during stress has been extensively studied in mammals, but least explored in lower vertebrates. The present in vitro study for the first time reports the specific opioid receptor-mediated immunomodulatory role of dynorphin-A((1-17)) in ectotherms. Dynorphin-A((1-17)) had pleiotropic effects on phagocyte functions, stimulatory on phagocytosis and superoxide production while inhibitory on the nitrite release. However, the effect of dynorphin-A((1-17)), whether stimulatory or inhibitory, markedly declined at high (10(-5)M) concentration. Dynorphin-A((1-17)) seems to mediate its action through opioid receptors since non-selective opioid receptor antagonist, naltrexone, completely blocked the effect of dynorphin-A((1-17)) on phagocytosis, superoxide production and nitrite release. Moreover, among specific opioid receptors antagonists, only selective kappa (kappa)-opioid receptor antagonist norbinaltorphimine was capable to antagonize the pleiotropic effects on phagocyte functions. The present study provides the direct evidence of immunomodulatory role of dynorphin-A((1-17)) via kappa-opioid receptor in freshwater teleost Channa punctatus.

摘要

内源性阿片肽在应激时释放,其在哺乳动物中的免疫调节作用已得到广泛研究,但在低等脊椎动物中研究甚少。本体外研究首次报道了强啡肽-A((1-17))在变温动物中特异性阿片受体介导的免疫调节作用。强啡肽-A((1-17))对吞噬细胞功能具有多效性影响,可刺激吞噬作用和超氧化物产生,同时抑制亚硝酸盐释放。然而,强啡肽-A((1-17))的作用(无论是刺激还是抑制)在高浓度(10(-5)M)时明显下降。强啡肽-A((1-17))似乎通过阿片受体介导其作用,因为非选择性阿片受体拮抗剂纳曲酮完全阻断了强啡肽-A((1-17))对吞噬作用、超氧化物产生和亚硝酸盐释放的影响。此外,在特异性阿片受体拮抗剂中,只有选择性κ(kappa)-阿片受体拮抗剂诺比那肽能够拮抗强啡肽-A((1-17))对吞噬细胞功能的多效性作用。本研究为淡水鱼类 Channa punctatus 中强啡肽-A((1-17))通过κ-阿片受体发挥免疫调节作用提供了直接证据。

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