The role of NMDA glutamate receptors in lung injury caused by chronic long-term intermittent hypobaric hypoxia

Chronic intermittent hypoxia (CIH), a component of sleep apnea-hypopnea syndrome, is suggested to cause damage to lung tissue, and the role of glutamate is not well studied. We used a chronic long-term intermittent hypobaric hypoxia (CLTIHH) model of rats to find out if such procedure causes lung in...

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Bibliographic Details
Published in:Brazilian journal of medical and biological research 2023-01, Vol.56 (1), p.e12549-e12549
Main Authors: Yaman, M O, Sönmez, O F, Ekiz-Yilmaz, T, Sönmez, D, Meydanlı, E E G, Guner, I, Sahin, G, Dariyerli, N, Yelmen, N
Format: Article
Language:eng ; por
Subjects:
Acute respiratory distress syndrome
Animals
BIOLOGY
Causes of
Complications and side effects
Development and progression
Dizocilpine Maleate - pharmacology
Glutamic Acid
Health aspects
Hypoxia
Hypoxia - complications
Interleukin-6 - metabolism
Lung Injury
MEDICINE, RESEARCH & EXPERIMENTAL
Methyl aspartate
N-Methylaspartate - pharmacology
Neurotransmitter receptors
Oxidants - pharmacology
Oxidative Stress
Rats
Receptors, Glutamate
Receptors, N-Methyl-D-Aspartate
Tumor Necrosis Factor-alpha - pharmacology
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Summary:Chronic intermittent hypoxia (CIH), a component of sleep apnea-hypopnea syndrome, is suggested to cause damage to lung tissue, and the role of glutamate is not well studied. We used a chronic long-term intermittent hypobaric hypoxia (CLTIHH) model of rats to find out if such procedure causes lung injury and the potential effect of N-methyl-D-aspartate receptors (NMDARs) by using receptor antagonist MK-801 (dizocilpine). Thirty-two rats were placed into four groups; a control and three CLTIHH groups where rats were placed into a low-pressure chamber set to 430 mmHg for 5 h/day, 5 days/week, for 5 weeks. Only one group received MK-801 (0.3 mg/kg, ip) daily. We evaluated tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, and nuclear factor (NF)-kB for the inflammatory process, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GPX), total antioxidant status (TAS), and total oxidant status (TOS) for oxidative stress, and caspase-9 levels. Blood plasma, bronchoalveolar fluid (BALF), and lung tissue extracts were evaluated. Both oxidant and inflammatory parameters were significantly increased in all the mediums of the CLTIHH groups except the group that received MK-801. Significant evidence was collected on MK-801 alleviating the effect of CLTIHH. Histological evaluations revealed lung damage and fibrotic changes in the CLTIHH groups. It was first shown that the CLTIHH procedure caused chronic lung injury, and that inflammation and oxidant stress were influential in the formation of lung injury. Secondly, NMDAR antagonist MK-801 effectively inhibited the development of lung injury and fibrosis.
ISSN:0100-879X
1414-431X
1414-431X
DOI:10.1590/1414-431X2023e12549