Hydrogen gas inhalation improves delayed brain injury by alleviating early brain injury after experimental subarachnoid hemorrhage

Molecular hydrogen (H ) protect neurons against reactive oxygen species and ameliorates early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study investigated the effect of H on delayed brain injury (DBI) using the rat SAH + unilateral common carotid artery occlusion (UCCAO) model wit...

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Bibliographic Details
Published in:Scientific reports 2020-07, Vol.10 (1), p.12319-12319, Article 12319
Main Authors: Kumagai, Kosuke, Toyooka, Terushige, Takeuchi, Satoru, Otani, Naoki, Wada, Kojiro, Tomiyama, Arata, Mori, Kentaro
Format: Article
Language:English
Subjects:
Administration, Inhalation
Anesthesia
Animals
Blood Pressure
Brain - metabolism
Brain - pathology
Brain - physiopathology
Brain Edema - complications
Brain Edema - physiopathology
Brain Injuries - drug therapy
Brain Injuries - etiology
Brain Injuries - physiopathology
Brain injury
c-Jun protein
Calcium-binding protein
Cardiovascular system
Carotid artery
Cell Death
Cerebral Arteries - pathology
Cerebral Arteries - physiopathology
Cerebral blood flow
Cerebrovascular Circulation
Edema
Gliosis
Gliosis - complications
Gliosis - pathology
Gliosis - physiopathology
Hydrogen
Hydrogen - administration & dosage
Hydrogen - therapeutic use
Inhalation
Intracranial Pressure
Ischemia
JNK Mitogen-Activated Protein Kinases - metabolism
JNK protein
Male
Neurological diseases
Neurons - pathology
Phosphorylation
Protein B
Rats, Sprague-Dawley
Reactive oxygen species
S100 Proteins - metabolism
S100b protein
Subarachnoid hemorrhage
Subarachnoid Hemorrhage - complications
Subarachnoid Hemorrhage - physiopathology
Time Factors
Transcription factors
Traumatic brain injury
Vasoconstriction
Vasospasm, Intracranial - pathology
Vasospasm, Intracranial - physiopathology
Water
Weight Loss
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Summary:Molecular hydrogen (H ) protect neurons against reactive oxygen species and ameliorates early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study investigated the effect of H on delayed brain injury (DBI) using the rat SAH + unilateral common carotid artery occlusion (UCCAO) model with the endovascular perforation method. 1.3% H gas (1.3% hydrogen premixed with 30% oxygen and balanced nitrogen) inhalation was performed on days 0 and 1, starting from anesthesia induction and continuing for 2 h on day 0, and starting from anesthesia induction and continuing for 30 min on day 1. EBI was assessed on the basis of brain edema, expression of S100 calcium-binding protein B (S100B), and phosphorylation of C-Jun N-terminal kinase on day 2, and neurological deficits on day 3. Reactive astrogliosis and severity of cerebral vasospasm (CV) were assessed on days 3 and 7. DBI was assessed on the basis of neurological deficits and neuronal cell death on day 7. EBI, reactive astrogliosis, and DBI were ameliorated in the H group compared with the control group. CV showed no significant improvement between the control and H groups. This study demonstrated that H gas inhalation ameliorated DBI by reducing EBI without improving CV in the rat SAH + UCCAO model.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-020-69028-5