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首页> 外文期刊>Life sciences >ELECTRON PARAMAGNETIC RESONANCE INVESTIGATIONS OF NITROSYL COMPLEX FORMATION DURING ENDOTOXIN TOLERANCE
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ELECTRON PARAMAGNETIC RESONANCE INVESTIGATIONS OF NITROSYL COMPLEX FORMATION DURING ENDOTOXIN TOLERANCE

机译：内毒素耐受过程中亚硝酰基复合物形成的电子顺磁共振研究

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The prior administration of low dose endotoxin induces a state of hyporesponsiveness or tolerance to the lethal effects of endotoxin. It is generally accepted that macrophages are main cellular components in the development of tolerance, hence, nitric oxide ((NO)-N-.) as one of the macrophage mediators may play a role in host defense mechanisms during tolerance. In this study, we utilized EPR spectroscopy to directly detect nitrosyl complexes as products of (NO)-N-. in whole blood, livers and intestines of lipopolysaccharide (LPS)-tolerant rats. Male Sprague-Dawley rats were injected with a ''low dose'' LPS (0.5 mg/kg) 12-168 h prior to a ''high dose'' LPS (3 mg/kg), then sacrificed 6 h later. EPR signals of nitrosyl hemoprotein complexes were detected in specimens after high dose LPS. The post-LPS EPR signals-of nitrosyl complexes from all samples were attenuated by a prior injection of low dose LPS. The signals of dinitrosyl-iron-dithiolate became apparent in samples from tolerant rats as signals of nitrosyl hemoprotein decreased. The maximal tolerance in terms of diminished (NO)-N-. production was observed when low dose LPS was given 48-96 h prior to high dose LPS. Hemoglobin concentrations in the intestine used as biomarkers of hemorrhagic damage, were concomitantly attenuated in the jejunum of tolerant rats. These results together with our previous studies indicate that suppression of (NO)-N-. production may contribute to the amelioration of hepatic and intestinal injury during endotoxin tolerance. [References: 35]
机译：预先给予低剂量内毒素会引起对内毒素致死作用的反应不足或耐受状态。普遍认为巨噬细胞是耐受性发展中的主要细胞成分，因此，作为巨噬细胞介体之一的一氧化氮（（NO）-N-。）可能在耐受过程中在宿主防御机制中发挥作用。在这项研究中，我们利用EPR光谱法直接检测作为（NO）-N-产物的亚硝酰基配合物。在耐受脂多糖（LPS）的大鼠的全血，肝脏和肠中。在“高剂量” LPS（3 mg / kg）之前12-168小时，对雄性Sprague-Dawley大鼠注射“低剂量” LPS（0.5 mg / kg），然后在6 h后处死。高剂量LPS​​后在标本中检测到亚硝酰血蛋白复合物的EPR信号。来自所有样品的亚硝酰基复合物的LPS后EPR信号被预先注入的低剂量LPS​​减弱。随着亚硝基血红蛋白信号的降低，二硝基亚铁二硫代铁的信号在耐受性大鼠的样品中变得明显。 （NO）-N-减小时的最大公差。当在高剂量LPS​​之前48-96小时给予低剂量LPS​​时，会观察到生产。在耐受性大鼠的空肠中，肠道中的血红蛋白浓度被用作出血损伤的生物标志物，其浓度随之降低。这些结果与我们以前的研究一起表明抑制（NO）-N-。内毒素耐受过程中产生的肝素可能有助于减轻肝脏和肠道损伤。 [参考：35]

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