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应激和甲硫氨酸脑啡肽对两种近交系大鼠巨噬细胞功能的影响。

The influence of stress and methionine-enkephalin on macrophage functions in two inbred rat strains.

作者信息

Stanojević Stanislava, Mitić Katarina, Vujić Vesna, Kovacević-Jovanović Vesna, Dimitrijević Mirjana

机构信息

Immunology Research Center Branislav Janković, Institute of Immunology and Virology Torlak, Vojvode Stepe 458, 11152 Belgrade, Serbia.

出版信息

Life Sci. 2007 Feb 13;80(10):901-9. doi: 10.1016/j.lfs.2006.11.019. Epub 2006 Nov 17.

Abstract

The aim of our current study was to investigate the effect of acute exposure to electric tail shock stress (ES) and to a stress witnessing procedure (SW), as models for physical and psychological stress paradigms, respectively, on phagocytosis and H(2)O(2) production in peritoneal macrophages isolated from Albino Oxford (AO) and Dark Agouti (DA) rats. In addition, we studied the in vitro effects of methionine-enkephalin (ME) on phagocytosis and H(2)O(2) production in peritoneal macrophages isolated from both AO and DA rats that had been exposed to ES and SW procedures. The results showed that peritoneal macrophages isolated from DA rats were less sensitive to the suppressive effects of ES and SW than macrophages isolated from AO rats. In vitro treatment of macrophages isolated from AO rats with ME mimicked to some extent the suppressive effects of ES and SW on phagocytosis and H(2)O(2) production and additionally diminished H(2)O(2) release in macrophages isolated from AO rats previously exposed to ES or SW. ME did not have any effect on phagocytosis in macrophages isolated from DA rats, but changed H(2)O(2) production in a concentration-dependent manner. In macrophages isolated from DA rats previously exposed to stress the effect of ME was dependent on the macrophage function tested and the particular stress paradigm employed. Our results emphasise the fact that both beneficial and detrimental effects of stress on immune system functions could be attributed to the individual variations in the macrophage's response to stress mediators.

摘要

我们当前研究的目的是分别以电尾休克应激(ES)和应激目睹程序(SW)作为身体和心理应激范式的模型,研究急性暴露于这两种应激对从白化牛津(AO)大鼠和黑褐大鼠(DA)分离的腹腔巨噬细胞吞噬作用和过氧化氢(H₂O₂)生成的影响。此外,我们研究了甲硫氨酸脑啡肽(ME)对已暴露于ES和SW程序的AO和DA大鼠分离的腹腔巨噬细胞吞噬作用和H₂O₂生成的体外影响。结果表明,与从AO大鼠分离的巨噬细胞相比,从DA大鼠分离的腹腔巨噬细胞对ES和SW的抑制作用不太敏感。用ME对从AO大鼠分离的巨噬细胞进行体外处理,在一定程度上模拟了ES和SW对吞噬作用和H₂O₂生成的抑制作用,并且还减少了先前暴露于ES或SW的AO大鼠分离的巨噬细胞中H₂O₂的释放。ME对从DA大鼠分离的巨噬细胞的吞噬作用没有任何影响,但以浓度依赖的方式改变了H₂O₂的生成。在先前暴露于应激的DA大鼠分离的巨噬细胞中,ME的作用取决于所测试的巨噬细胞功能和所采用的特定应激范式。我们的结果强调了这样一个事实,即应激对免疫系统功能产生的有益和有害影响都可能归因于巨噬细胞对应激介质反应的个体差异。

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