Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver
Sleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2012/879419 |
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| author | Darlan Pase da Rosa Luiz Felipe Forgiarini Diego Baronio Cristiano Andrade Feijó Dênis Martinez Norma Possa Marroni |
| author_facet | Darlan Pase da Rosa Luiz Felipe Forgiarini Diego Baronio Cristiano Andrade Feijó Dênis Martinez Norma Possa Marroni |
| author_sort | Darlan Pase da Rosa |
| collection | DOAJ |
| description | Sleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and nonalcoholic steatohepatitis. We assessed the level of inflammation in the lung and liver tissue from animals subjected to intermittent hypoxia and simulated sleep apnea. A total of 12 C57BL/6 mice were divided into two groups and then exposed to IH (n=6) or a simulated IH (SIH) (n=6) for 35 days. We observed an increase in oxidative damage and other changes to endogenous antioxidant enzymes in mice exposed to IH. Specifically, the expression of multiple transcription factors, including hypoxia inducible factor (HIF-1α), nuclear factor kappa B (NF-κB), and tumor necrosis factor (TNF-α), inducible NO synthase (iNOS), vascular endothelial growth factor (VEGF), and cleaved caspase 3 were shown to be increased in the IH group. Overall, we found that exposure to intermittent hypoxia for 35 days by simulating sleep apnea leads to oxidative stress, inflammation, and increased activity of caspase 3 in the liver and lung. |
| format | Article |
| id | doaj-art-44e15c04fd7e43139b28e2acd519d6d2 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-44e15c04fd7e43139b28e2acd519d6d22025-08-20T03:36:44ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/879419879419Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and LiverDarlan Pase da Rosa0Luiz Felipe Forgiarini1Diego Baronio2Cristiano Andrade Feijó3Dênis Martinez4Norma Possa Marroni5Ciências Médicas, Programa de Pós-Graduação em Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, BrazilHospital de Clínicas de Porto Alegre (HCPA), Universidade Federal do Rio Grande do Sul, 90035-903 Porto Alegre, RS, BrazilCiências Médicas, Programa de Pós-Graduação em Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, BrazilHospital de Clínicas de Porto Alegre (HCPA), Universidade Federal do Rio Grande do Sul, 90035-903 Porto Alegre, RS, BrazilCiências Médicas, Programa de Pós-Graduação em Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, BrazilCiências Médicas, Programa de Pós-Graduação em Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, BrazilSleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and nonalcoholic steatohepatitis. We assessed the level of inflammation in the lung and liver tissue from animals subjected to intermittent hypoxia and simulated sleep apnea. A total of 12 C57BL/6 mice were divided into two groups and then exposed to IH (n=6) or a simulated IH (SIH) (n=6) for 35 days. We observed an increase in oxidative damage and other changes to endogenous antioxidant enzymes in mice exposed to IH. Specifically, the expression of multiple transcription factors, including hypoxia inducible factor (HIF-1α), nuclear factor kappa B (NF-κB), and tumor necrosis factor (TNF-α), inducible NO synthase (iNOS), vascular endothelial growth factor (VEGF), and cleaved caspase 3 were shown to be increased in the IH group. Overall, we found that exposure to intermittent hypoxia for 35 days by simulating sleep apnea leads to oxidative stress, inflammation, and increased activity of caspase 3 in the liver and lung.http://dx.doi.org/10.1155/2012/879419 |
| spellingShingle | Darlan Pase da Rosa Luiz Felipe Forgiarini Diego Baronio Cristiano Andrade Feijó Dênis Martinez Norma Possa Marroni Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver Mediators of Inflammation |
| title | Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver |
| title_full | Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver |
| title_fullStr | Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver |
| title_full_unstemmed | Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver |
| title_short | Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver |
| title_sort | simulating sleep apnea by exposure to intermittent hypoxia induces inflammation in the lung and liver |
| url | http://dx.doi.org/10.1155/2012/879419 |
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