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实验性自身免疫性前列腺炎(EAP)大鼠腹膜巨噬细胞产生反应性氮中间产物(RNI)。

Production of reactive nitrogen intermediates (RNI) by peritoneal macrophages from rats with experimental autoimmune prostatitis (EAP).

作者信息

Orsilles M A, Depiante-Depaoli M

机构信息

Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Córdoba, Argentina.

出版信息

Inflammation. 1995 Aug;19(4):415-22. doi: 10.1007/BF01534576.

DOI:10.1007/BF01534576
PMID:7558247
Abstract

Peritoneal macrophages from experimental autoimmune prostatitis (EAP) rats were examined for their capacity to secrete reactive nitrogen intermediates (RNI), measured by the release of nitrite (NO2-). Under basal conditions, there was a significant increase of NO2- secretion by cells from autoimmune rats in relation to resident cells. After stimulation in vitro with lipopolysaccharide (LPS), the NO2- production was higher in cells from autoimmune rats compared to treated and nontreated controls. The NO2- production was dependent upon the presence of L-arginine in the culture medium. The addition of L-NG-monomethyl arginine, an inhibitor of nitric oxide synthesis, to the medium reduced the amount of measurable NO2-. Kinetic studies in cells from EAP rats showed that in basal conditions there was an significant release of NO2- at day 7 of immunization that was maintained during the whole period studied. After LPS stimulation, there was a similar behavior and maximum values were reached at day 28 of immunization. These results, together with the lesion observed in the prostate gland, suggest that RNI may be of pathogenic importance in the development of early tissue inflammation and autoimmune disease of the prostate.

摘要

对实验性自身免疫性前列腺炎(EAP)大鼠的腹膜巨噬细胞分泌反应性氮中间体(RNI)的能力进行了检测,通过亚硝酸盐(NO2-)释放量来衡量。在基础条件下,与驻留细胞相比,自身免疫大鼠的细胞分泌NO2-显著增加。体外经脂多糖(LPS)刺激后,与处理和未处理的对照相比,自身免疫大鼠的细胞中NO2-生成量更高。NO2-的生成依赖于培养基中L-精氨酸的存在。向培养基中添加一氧化氮合成抑制剂L-NG-单甲基精氨酸可减少可测量的NO2-量。对EAP大鼠细胞的动力学研究表明,在基础条件下,免疫第7天有显著的NO2-释放,且在整个研究期间持续存在。LPS刺激后,出现类似行为,免疫第28天达到最大值。这些结果,连同在前列腺中观察到的病变,表明RNI可能在前列腺早期组织炎症和自身免疫性疾病的发展中具有致病重要性。

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本文引用的文献

1
Experimental autoimmune prostatitis (EAP): enhanced release of reactive oxygen intermediates (ROI) in peritoneal macrophages.实验性自身免疫性前列腺炎(EAP):腹膜巨噬细胞中活性氧中间体(ROI)释放增加
Autoimmunity. 1993;16(3):201-7. doi: 10.3109/08916939308993328.
2
Engagement of major histocompatibility complex class II molecules leads to nitrite production in bone marrow-derived macrophages.主要组织相容性复合体II类分子的激活会导致骨髓来源的巨噬细胞产生亚硝酸盐。
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Testosterone metabolism in vitro by prostate homogenate from isoimmunized rats.
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Experimental autoimmune damage to rat male accessory glands. I. Transfer of autoimmune response by spleen cells.大鼠雄性附属性腺的实验性自身免疫损伤。I. 脾细胞对自身免疫反应的转移。
Am J Reprod Immunol (1980). 1984 Jan-Feb;5(1):9-14. doi: 10.1111/j.1600-0897.1984.tb00280.x.
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[Experimental autoimmunity against male accessory glands of rats. Correlation between specific tissular lesion and lymphocyte reactivity of thymus, bone marrow, spleen, ganglia and blood].[大鼠雄性附属性腺的实验性自身免疫。特定组织损伤与胸腺、骨髓、脾脏、神经节及血液中淋巴细胞反应性之间的相关性]
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