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睡眠片段化和血管紧张素 II 处理对小鼠促炎反应的对比影响。

Contrasting effects of sleep fragmentation and angiotensin-II treatment upon pro-inflammatory responses of mice.

机构信息

Department of Biology, Western Kentucky University, Bowling Green, KY, USA.

Department of Biological Sciences, San José State University, San Jose, CA, USA.

出版信息

Sci Rep. 2022 Aug 30;12(1):14763. doi: 10.1038/s41598-022-19166-9.

DOI:10.1038/s41598-022-19166-9
PMID:36042284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9427781/
Abstract

Disordered sleep promotes inflammation in brain and peripheral tissues, but the mechanisms that regulate these responses are poorly understood. One hypothesis is that activation of the sympathetic nervous system (SNS) from sleep loss elevates blood pressure to promote vascular sheer stress leading to inflammation. As catecholamines produced from SNS activation can directly regulate inflammation, we pharmacologically altered blood pressure using an alternative approach-manipulation of the renin-angiotensin system (RAS). Male C57BL6/J mice were treated with angiotensin or captopril to elevate and reduce blood pressure, respectively and then exposed to 24-h of sleep fragmentation (SF) or allowed to sleep (control). Pro- and anti-inflammatory cytokine gene expression and as endothelial adhesion gene expression as well as serum glucocorticoids (corticosterone) were measured. RAS manipulation elevated cytokines and endothelial adhesion expression in heart and aorta while SF increased cytokine expression in peripheral tissues, but not brain. However, there were interactive effects of angiotensin-II and SF upon cytokine gene expression in hippocampus and hypothalamus, but not prefrontal cortex. SF, but not RAS manipulation, elevated serum corticosterone concentration. These findings highlight the contrasting effects of RAS manipulation and SF, implying that inflammation from SF is acting on different pathways that are largely independent of RAS manipulation.

摘要

睡眠紊乱会促进大脑和外周组织的炎症反应,但调节这些反应的机制还不甚清楚。有一个假说认为,睡眠剥夺会激活交感神经系统(SNS),从而使血压升高,促进血管壁剪切力增加,导致炎症。由于 SNS 激活产生的儿茶酚胺可以直接调节炎症,我们通过另一种方法——肾素-血管紧张素系统(RAS)的操作来改变血压。雄性 C57BL6/J 小鼠分别用血管紧张素或卡托普利处理以升高和降低血压,然后进行 24 小时的睡眠碎片化(SF)或允许睡眠(对照)。检测促炎和抗炎细胞因子基因表达以及内皮黏附基因表达和血清糖皮质激素(皮质酮)浓度。RAS 操作增加了心脏和主动脉中的细胞因子和内皮黏附表达,而 SF 增加了外周组织中的细胞因子表达,但不增加大脑中的细胞因子表达。然而,血管紧张素 II 和 SF 对海马和下丘脑细胞因子基因表达有交互作用,但对前额叶皮层没有影响。SF 而不是 RAS 操作会增加血清皮质酮浓度。这些发现突出了 RAS 操作和 SF 的对比作用,表明 SF 引起的炎症作用于不同的途径,这些途径在很大程度上独立于 RAS 操作。

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本文引用的文献

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2
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Am J Physiol Regul Integr Comp Physiol. 2020 Apr 1;318(4):R781-R789. doi: 10.1152/ajpregu.00358.2019. Epub 2020 Mar 4.
3
Metabolic control and sex: A focus on inflammatory-linked mediators.
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PLoS One. 2023 Dec 14;18(12):e0288889. doi: 10.1371/journal.pone.0288889. eCollection 2023.
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