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Published in: Inflammation Research 1/2015

01-01-2015 | Original Research Paper

Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea

Authors: Darlan Pase da Rosa, Luiz Felipe Forgiarini, Mariel Barbachan e Silva, Cíntia Zappe Fiori, Cristiano Feijó Andrade, Dênis Martinez, Norma Possa Marroni

Published in: Inflammation Research | Issue 1/2015

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Abstract

Background

Sleep apnea causes intermittent hypoxia (IH). We aimed to investigate the proteins related to oxidative stress, inflammation and apoptosis in liver tissue subjected to IH as a simulation of sleep apnea in conjunction with the administration of either melatonin (MEL, 200 μL/kg) or N-acetylcysteine (NAC, 10 mg/kg).

Methods

Seventy-two adult male Balb-C mice were divided: simulation of IH (SIH), SIH + MEL, SIH + NAC, IH, IH + MEL and IH + NAC. The animals were subjected to simulations of sleep apnea for 8 h a day for 35 days. The data were analyzed with ANOVA and Tukey tests with the significance set at p < 0.05.

Results

In IH, there was a significant increase in oxidative stress and expression of HIF-1a. In addition, we observed increase in the activation levels of NF-kB. This increase may be responsible for the increased expression of TNF-alpha and iNOS as well as the significant increase of VEGF signaling and expression of caspase-3 and caspase-6, which suggests an increase in apoptosis. In the groups treated with antioxidants, the analysis showed that the enzyme activity and protein levels were similar to those of the non-simulated group.

Conclusions

Thus, we show that IH causes liver inflammation and apoptosis, which may be protected with either MEL or NAC.
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Metadata
Title
Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea
Authors
Darlan Pase da Rosa
Luiz Felipe Forgiarini
Mariel Barbachan e Silva
Cíntia Zappe Fiori
Cristiano Feijó Andrade
Dênis Martinez
Norma Possa Marroni
Publication date
01-01-2015
Publisher
Springer Basel
Published in
Inflammation Research / Issue 1/2015
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-014-0778-5

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