Hydrogen Gas Protects Newborn Brain from Birth Asphyxia Damage
- Authors
- Viktória Varga, János Németh, Orsolya Oláh, Valéria Tóth-Szűki, Viktória Kovács, Gábor Remzső, Ferenc Domoki
- Journal
- Acta Pharmacologica Sinica
- Year
- 2018
- DOI
- 10.1038/aps.2017.148
- Study Type
- Pig
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Hungary
- Health Condition
- Hypoxic-Ischemic Encephalopathy
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas reduced brain inflammation and damage in newborn pigs that experienced severe lack of oxygen.
Key Finding
Hydrogen gas treatment prevented the rise in COX-2 protein expression in the brains of newborn pigs with severe oxygen deprivation, and reduced markers of oxidative stress and inflammation in brain tissue.
Summary
Researchers studied newborn pigs that experienced severe oxygen deprivation (asphyxia) to see if hydrogen gas could protect their brains. They found that asphyxia triggered increased production of a protein called COX-2 in specific brain regions, which is known to contribute to brain damage. When piglets were treated with hydrogen gas (inhaled for 4 hours), the harmful increase in COX-2 was largely prevented, and markers of brain inflammation and oxidative stress (cellular damage from unstable molecules) were reduced.
Practical Takeaway
This animal study suggests hydrogen gas may protect newborn brains from damage caused by oxygen deprivation by reducing inflammation and oxidative stress. However, this research was conducted only in pigs, not humans, so it remains unclear whether these protective effects would occur in human infants. Much more research, including human trials, would be needed before hydrogen therapy could be considered for treating birth-related brain injuries.
Abstract
Cyclooxygenase-2 (COX-2) has an established role in the pathogenesis of hypoxic-ischemic encephalopathy (HIE). In this study we sought to determine whether COX-2 was induced by asphyxia in newborn pigs, and whether neuronal COX-2 levels were affected by H2 treatment. Piglets were subjected to either 8 min of asphyxia or a more severe 20 min of asphyxia followed by H2 treatment (inhaling room air containing 2.1% H2 for 4 h). COX-2 immunohistochemistry was performed on brain samples from surviving piglets 24 h after asphyxia. The percentages of COX-2-immunopositive neurons were determined in cortical and subcortical areas. Only in piglets with more severe HIE, we observed significant, region-specific increases in neuronal COX-2 expression within the parietal and occipital cortices and in the CA3 hippocampal subfield. H2 treatment essentially prevented the increases in COX-2-immunopositive neurons. In the parietal cortex, the attenuation of COX-2 induction was associated with reduced 8'-hydroxy-2'-deoxyguanozine immunoreactivity and retained microglial ramifcation index, which are markers of oxidative stress and neuroinfiammation, respectively. This study demonstrates for the first time that asphyxia elevates neuronal COX-2 expression in a piglet HIE model. Neuronal COX-2 induction may play region-specific roles in brain lesion progression during HIE development, and inhibition of this response may contribute to the antioxidant/anti-infiammatory neuroprotective effects of H2 treatment.