scholarly journals Chronic intermittent hypoxia increases rat sternohyoid muscle NADPH oxidase expression with attendant modest oxidative stress

2015 ◽  
Vol 6 ◽  
Author(s):  
Robert Williams ◽  
Paul Lemaire ◽  
Philip Lewis ◽  
Fiona B. McDonald ◽  
Eric Lucking ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia

scholarly journals NADPH Oxidase Is Required for the Sensory Plasticity of the Carotid Body by Chronic Intermittent Hypoxia

2009 ◽  
Vol 29 (15) ◽  
pp. 4903-4910 ◽  
Author(s):  
Y.- J. Peng ◽  
J. Nanduri ◽  
G. Yuan ◽  
N. Wang ◽  
E. Deneris ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Sensory Plasticity

scholarly journals Chronic intermittent hypoxia induces hypoxic sensitivity in adult rat adrenal medulla via oxidative stress

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Ganesh K Kumar ◽  
Vandana Rai ◽  
Suresh Sharma ◽  
DeviPrasadh Ramakrishnan ◽  
Ying‐Jie Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adrenal Medulla ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Adult Rat

Hydrogen ameliorates chronic intermittent hypoxia-induced neurocognitive impairment via inhibiting oxidative stress

2018 ◽  
Vol 143 ◽  
pp. 225-233 ◽  
Author(s):  
Wenya Li ◽  
Shengchang Yang ◽  
Fu-Yang Yu ◽  
Yashuo Zhao ◽  
Zhi-Min Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Neurocognitive Impairment ◽  
Chronic Intermittent Hypoxia

scholarly journals Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1184 ◽  
Author(s):  
Peng Guan ◽  
Zhi-Min Sun ◽  
Li-Fei Luo ◽  
Ya-Shuo Zhao ◽  
Sheng-Chang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Renal Injury ◽  
Intermittent Hypoxia ◽  
Hydrogen Gas ◽  
Chronic Intermittent Hypoxia ◽  
Protective Effects ◽  
Divalent Metal Transporter 1 ◽  
Divalent Metal Transporter ◽  
And Oxidative Stress

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

scholarly journals Chronic intermittent hypoxia induces hypoxia-evoked catecholamine efflux in adult rat adrenal medulla via oxidative stress

2006 ◽  
Vol 575 (1) ◽  
pp. 229-239 ◽  
Author(s):  
Ganesh K. Kumar ◽  
Vandana Rai ◽  
Suresh D. Sharma ◽  
Devi Prasadh Ramakrishnan ◽  
Ying-Jie Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adrenal Medulla ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Adult Rat

scholarly journals Intermittent Hypoxia Increases the Severity of Bleomycin-Induced Lung Injury in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Thomas Gille ◽  
Morgane Didier ◽  
Cécile Rotenberg ◽  
Eva Delbrel ◽  
Dominique Marchant ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Fibrosis ◽  
Pulmonary Edema ◽  
Cell Apoptosis ◽  
Lung Fibrosis ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Obstructive Sleep ◽  
The Impact ◽  
Lung Oxidative Stress

Background. Severe obstructive sleep apnea (OSA) with chronic intermittent hypoxia (IH) is common in idiopathic pulmonary fibrosis (IPF). Here, we evaluated the impact of IH on bleomycin- (BLM-) induced pulmonary fibrosis in mice. Methods. C57BL/6J mice received intratracheal BLM or saline and were exposed to IH (40 cycles/hour; FiO2 nadir: 6%; 8 hours/day) or intermittent air (IA). In the four experimental groups, we evaluated (i) survival; (ii) alveolar inflammation, pulmonary edema, lung oxidative stress, and antioxidant enzymes; (iii) lung cell apoptosis; and (iv) pulmonary fibrosis. Results. Survival at day 21 was lower in the BLM-IH group (p<0.05). Pulmonary fibrosis was more severe at day 21 in BLM-IH mice, as assessed by lung collagen content (p=0.02) and histology. At day 4, BLM-IH mice developed a more severe neutrophilic alveolitis, (p<0.001). Lung oxidative stress was observed, and superoxide dismutase and glutathione peroxidase expression was decreased in BLM-IH mice (p<0.05 versus BLM-IA group). At day 8, pulmonary edema was observed and lung cell apoptosis was increased in the BLM-IH group. Conclusion. These results show that exposure to chronic IH increases mortality, lung inflammation, and lung fibrosis in BLM-treated mice. This study raises the question of the worsening impact of severe OSA in IPF patients.

scholarly journals Silencing MR-1 Protects against Myocardial Injury Induced by Chronic Intermittent Hypoxia by Targeting Nrf2 through Antioxidant Stress and Anti-Inflammation Pathways

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Qixue Wang ◽  
Yue Wang ◽  
Jiner Zhang ◽  
Shuo Pan ◽  
Shaofeng Liu
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Myocardial Injury ◽  
Cardiac Insufficiency ◽  
Inflammatory Factors ◽  
Chronic Intermittent Hypoxia ◽  
Heme Oxygenase 1 ◽  
Stress System ◽  
Antioxidant Stress ◽  
And Oxidative Stress

Background. Patients with obstructive sleep apnea hypopnea syndrome (OSAHS) often have cardiac insufficiency mainly due to hypoxia/reperfusion injury caused by chronic intermittent hypoxia (CIH). Inflammation and oxidative stress are involved in the cardiovascular events of OSAHS patients. Studies have found that myofibrillation regulator-1 (MR-1) participates in the pathological process of OSAHS-induced myocardial injury, but the specific mechanism is still unclear. Methods. We used a CIH-induced rat model to simulate the process of OSAHS disease. Indices of myocardial injury, inflammation, and oxidative stress were detected using quantitative PCR and enzyme-linked immunosorbent assay (ELISA). After administration of adenoassociated viral vector (AAV) encoding silencing RNA against MR-1, we examined expression of the classic antioxidant stress pathway protein NF-E2-related factor 2 (Nrf2) using western blotting. Results. We found that levels of serum inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 were increased, and we further observed disturbance of the oxidative stress system, in which the content of reactive oxygen species (ROS), superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA) was enhanced in CIH-induced rats. Subsequently, we detected that expression of Nrf2 and heme oxygenase-1 (HO-1) was slightly increased, while the expression of Kelch-like ECH-associated protein 1 (Keap-1) was significantly increased in the CIH model. Interestingly, after administration of silencing MR-1 AAV, the elevated levels of inflammatory factors were reduced, and the disordered oxidative stress system was corrected. Additionally, the expression of Nrf2 and HO-1 was distinctly increased, but the high expression of Keap-1 was decreased. Conclusions. Our research results demonstrate that silencing MR-1 rescued the myocardium the injury from inflammatory and oxidative stress in CIH-induced rats by administration of the Nrf2 signaling pathway.

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