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.
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.
Authors: Vladimir Savransky; Ashika Nanayakkara; Angelica Vivero; Jianguo Li; Shannon Bevans; Philip L Smith; Michael S Torbenson; Vsevolod Y Polotsky Journal: Hepatology Date: 2007-04 Impact factor: 17.425
Authors: Martin Feelisch; Bernadette O Fernandez; Nathan S Bryan; Maria Francisca Garcia-Saura; Selena Bauer; David R Whitlock; Peter C Ford; David R Janero; Juan Rodriguez; Houman Ashrafian Journal: J Biol Chem Date: 2008-10-03 Impact factor: 5.157
Authors: Shikha S Sundaram; Ann Halbower; Zhaoxing Pan; Kristen Robbins; Kelley E Capocelli; Jelena Klawitter; Colin T Shearn; Ronald J Sokol Journal: J Hepatol Date: 2016-08-05 Impact factor: 25.083
Authors: Ruben Manuel Luciano Colunga Biancatelli; Max Berrill; Yassen H Mohammed; Paul E Marik Journal: J Thorac Dis Date: 2020-02 Impact factor: 2.895