Atorvastatin attenuates intermittent hypoxia-induced myocardial oxidative stress in a mouse obstructive sleep apnea model
Autor: | Hui-Qing Zeng, Yan Chen, Xiao-Bin Zhang, Kam Yu Chiu, Hui-Juan Cheng, Ya-Ting Yuan, Yi-Yuan Chen |
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Rok vydání: | 2021 |
Předmět: |
Male
Aging medicine.medical_specialty Antioxidant NF-E2-Related Factor 2 medicine.medical_treatment Atorvastatin intermittent hypoxia Myocardial Ischemia Superoxide dismutase activity medicine.disease_cause Mice chemistry.chemical_compound Internal medicine medicine Animals Hypoxia Sleep Apnea Obstructive business.industry apoptosis Heart Intermittent hypoxia atorvastatin myocardial Cell Biology Malondialdehyde medicine.disease Mice Inbred C57BL Obstructive sleep apnea Disease Models Animal Oxidative Stress Endocrinology chemistry Apoptosis business Oxidative stress Research Paper medicine.drug |
Zdroj: | Aging (Albany NY) |
ISSN: | 1945-4589 |
Popis: | Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), is associated with various cardiovascular diseases. In the present study, we assessed the effect of the lipid reducing agent atorvastatin on CIH-induced myocardial oxidative stress and apoptosis in a mouse OSA model. Forty-eight C57BL/6J mice were evenly divided among normoxia + vehicle, normoxia + atorvastatin, CIH + vehicle, and CIH + atorvastatin groups. CIH consisted of a hypoxia-reoxygenation cycle in which oxygen concentrations fluctuated from 21% to 6% and back over two minutes for 8 hours each day (30 events/hour). CIH exposure continued for 12 weeks. Atorvastatin (5 mg/kg) was administered from week 6 through the end of the experiment. CIH increased malondialdehyde levels and decreased superoxide dismutase activity, total antioxidant capacity, and nuclear factor erythroid 2-related factor 2 levels in cardiac tissue, indicating a reduction in antioxidant activity. Atorvastatin significantly reversed those effects (p < 0.05). CIH also increased B-cell lymphoma 2-associated protein X and cleaved caspased-3 levels as well as the myocardial apoptotic rate, as indicated by terminal deoxynucleotidyl transferase dUTP nick-end labeling. Atorvastatin had no effect on those changes (p > 0.05). Thus, atorvastatin administration exerts antioxidant but not anti-apoptotic effects after CIH and may therefore have therapeutic potential in OSA patients with cardiovascular comorbidities. |
Databáze: | OpenAIRE |
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