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Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

机译:间歇性缺氧暴露的气肿大鼠的系统性和内皮炎症和内皮祖细胞水平

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BACKGROUND: This study aimed to develop an overlap syndrome rat model with intermittent hypoxia (IH) exposure as seen in obstructive sleep apnea, on a base of preexisting emphysema caused by 16 wk of smoke exposure to determine whether IH and emphysema existing simultaneously play overlapped roles on systematic/endothelial inflammation and endothelial damage. METHODS: Sixty male Wistar rats were divided into 4 groups of 15 each, labeled according to exposure conditions as control, IH, emphysema, and overlap groups. In these animals, electroencephalogram monitoring and preliminary experiments to obtain arterial blood gas values were performed. Serum concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, TNF-alpha and IL-6 concentrations in the culture medium, Ras homology A mRNA expression levels of endothelial cells from right common carotid artery, and ratio of carotid intima-media thickness of whole thickness of vascular wall expressed in percent (C-IMT) (%) values were evaluated. Subsequently, circulating endothelial progenitor cells (EPCs) within rat peripheral blood and bone marrow were measured with flow cytometry. RESULTS: The serum and endothelial concentrations of TNF-alpha and IL-6 and the levels of endothelial Ras homology A mRNA have statistically significant results described as overlap > emphysema > IH > control. The levels of EPCs in rat peripheral blood and bone marrow have statistically significant results described as overlap > IH > emphysema > control. C-IMT (%) values from right common carotid artery are the highest in the overlap group and the lowest in the control group. There is no statistical difference when comparing the IH and the emphysema groups. CONCLUSIONS: Regardless of whether IH and emphysema exposure are mechanistically synergistic, this overlap elicits a more severe systematic/endothelial inflammation and endothelial damage; meanwhile, a robust mobilization of EPCs is demonstrated, which is not to mean a robust adherent and repairing capability. (C) 2015 Daedalus Enterprises
机译:背景:这项研究旨在建立一种阻塞性睡眠呼吸暂停中出现间歇性缺氧(IH)的重叠综合征大鼠模型,该模型以16周的烟尘暴露引起的肺气肿为基础,以确定IH和肺气肿是否同时发挥重叠作用对系统/内皮发炎和内皮损伤的影响。方法:将60只雄性Wistar大鼠分为4组,每组15只,根据暴露条件进行标记,分别作为对照组,IH,肺气肿和重叠组。在这些动物中,进行了脑电图监测和初步实验以获得动脉血气值。血清中肿瘤坏死因子(TNF)-α和白介素(IL)-6的血清浓度,培养基中TNF-α和IL-6的浓度,右颈总动脉内皮细胞Ras同源性A mRNA表达水平以及评估以百分比(C-IMT)(%)值表示的血管壁总厚度的颈动脉内膜中层厚度。随后,用流式细胞仪测量大鼠外周血和骨髓中的循环内皮祖细胞(EPC)。结果:血清和内皮细胞中TNF-α和IL-6的浓度以及内皮Ras同源性A mRNA的水平在统计学上具有显着意义,描述为重叠>肺气肿> IH>对照。大鼠外周血和骨髓中的EPCs水平具有统计学上显着的结果,描述为重叠> IH>肺气肿>对照。右颈总动脉的C-IMT(%)值在重叠组中最高,在对照组中最低。比较IH和肺气肿组没有统计学差异。结论:无论IH和肺气肿暴露是否具有机械协同作用,这种重叠都会引起更严重的系统/内皮炎症和内皮损伤。同时,展示了EPC的强大动员能力,但这并不意味着强大的附着力和修复能力。 (C)2015 Daedalus企业

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