Literature DB >> 25587169

Systematic and endothelial inflammation and endothelial progenitor cell levels in emphysematous rats exposed to intermittent hypoxia.

Qing-chan Yang1, Xin Sun1, Yong-mei Wang2, Qi Wu1, Jing Feng3, Bao-yuan Chen4.   

Abstract

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)-α and interleukin (IL)-6, TNF-α 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-α 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.
Copyright © 2015 by Daedalus Enterprises.

Entities:  

Keywords:  emphysema; endothelial dysfunction; endothelial progenitor cell; inflammation; intermittent hypoxia

Mesh:

Substances:

Year:  2015        PMID: 25587169     DOI: 10.4187/respcare.03492

Source DB:  PubMed          Journal:  Respir Care        ISSN: 0020-1324            Impact factor:   2.258


  5 in total

1.  Resveratrol Attenuates Intermittent Hypoxia-Induced Lung Injury by Activating the Nrf2/ARE Pathway.

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Journal:  Lung       Date:  2020-01-20       Impact factor: 2.584

Review 2.  The role of the endothelium in asthma and chronic obstructive pulmonary disease (COPD).

Authors:  Clara E Green; Alice M Turner
Journal:  Respir Res       Date:  2017-01-18

3.  Effects of Antioxidant Tempol on Systematic Inflammation and Endothelial Apoptosis in Emphysematous Rats Exposed to Intermittent Hypoxia.

Authors:  Haiyan Zhao; Yaping Zhao; Xin Li; Leiqian Xu; Fangxin Jiang; Wanju Hou; Lixia Dong; Jie Cao
Journal:  Yonsei Med J       Date:  2018-11       Impact factor: 2.759

4.  Endothelial function and T-lymphocyte subsets in patients with overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea.

Authors:  Juan Wang; Xin Li; Wan-Ju Hou; Li-Xia Dong; Jie Cao
Journal:  Chin Med J (Engl)       Date:  2019-07-20       Impact factor: 2.628

5.  Effect of the asthma-chronic obstructive pulmonary disease syndrome on the stroke, Parkinson's disease, and dementia: a national cohort study.

Authors:  Jun-Jun Yeh; Yu-Feng Wei; Cheng-Li Lin; Wu-Huei Hsu
Journal:  Oncotarget       Date:  2017-12-26
  5 in total

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