scholarly journals Atractylon treatment prevents sleep-disordered breathing-induced cognitive dysfunction by suppression of chronic intermittent hypoxia-induced M1 microglial activation

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Yan Lin ◽  
Xiuxiu Liu ◽  
Dan Tan ◽  
Zhiyan Jiang
Keyword(s):  
Protective Effect ◽  
Cognitive Dysfunction ◽  
Intermittent Hypoxia ◽  
Sleep Disordered Breathing ◽  
Microglial Activation ◽  
Cell Injury ◽  
Inflammatory Factors ◽  
Chronic Intermittent Hypoxia ◽  
Bv2 Cells ◽  
Disordered Breathing

Abstract Chronic intermittent hypoxia (CIH) induced by sleep-disordered breathing (SDB) is a key factor involved in cognitive dysfunction (CD). Increasing evidence has shown that atractylon (ATR) has anti-inflammatory effects. However, it remains unclear if ATR has a protective effect against SDB-induced nerve cell injury and CD. So, in the present study, CIH-exposed mice and CIH-induced BV2 cells were used to mimic SDB. The results showed that ATR treatment decreased CIH-induced CD and the expression of inflammatory factors in the hippocampal region by suppression of M1 microglial activation and promotion of M2 microglial activation. Also, ATR treatment promoted sirtuin 3 (SIRT3) expression. Down-regulation of SIRT3 decreased the protective effect of ATR against CIH-induced microglial cell injury. Furthermore, in vitro detection found that SIRT3 silencing suppressed ATR-induced M2 microglial activation after exposure to CIH conditions. Taken together, these results indicate that ATR treatment prevents SDB-induced CD by inhibiting CIH-induced M1 microglial activation, which is mediated by SIRT3 activation.

Protective effect of salidroside on cardiac apoptosis in mice with chronic intermittent hypoxia

2014 ◽  
Vol 174 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Mei-Chih Lai ◽  
Jaung-Geng Lin ◽  
Pei-Ying Pai ◽  
Mei-Hsin Lai ◽  
Yueh-Min Lin ◽  
...  
Keyword(s):  
Protective Effect ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Cardiac Apoptosis

Protective effect of adiponectin on genioglossus in mitophagy impaired by chronic intermittent hypoxia

2019 ◽  
Vol 64 ◽  
pp. S411-S412
Author(s):  
W. Wang ◽  
X. Zhang ◽  
Y. Zhu ◽  
N. Ding ◽  
H. Huang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia

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.

scholarly journals Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives

2008 ◽  
Vol 32 (4) ◽  
pp. 1082-1095 ◽  
Author(s):  
P. Levy ◽  
J-L. Pepin ◽  
C. Arnaud ◽  
R. Tamisier ◽  
J-C. Borel ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Sleep Disordered Breathing ◽  
Disordered Breathing

Cognitive Dysfunction in Children with Sleep-Disordered Breathing

2005 ◽  
Vol 20 (5) ◽  
pp. 400-404 ◽  
Author(s):  
Luciane Bizari Coin Carvalho ◽  
Lucila F. Prado ◽  
Luciana Silva ◽  
Marilaine Medeiros de Almeida ◽  
Tatiana Almeida e Silva ◽  
...  
Keyword(s):  
Cognitive Dysfunction ◽  
Sleep Disordered Breathing ◽  
Disordered Breathing
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