Hydrogen Gas Therapy Protects Newborn Brains After Oxygen Loss
- Authors
- Jianmei Cai, Zhimin Kang, Wen Wu Liu, Xu Luo, Sun Qiang, John H. Zhang, Shigeo Ohta, Xuejun Sun, Weigang Xu, Hengyi Tao, Runping Li
- Journal
- Neuroscience Letters
- Year
- 2008
- DOI
- 10.1016/j.neulet.2008.05.077
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Neonatal Hypoxia-Ischemia
- Body System
- Nervous System
TL;DR
Breathing hydrogen gas can help protect the brains of newborn rats from damage after a loss of blood flow and oxygen.
Key Finding
This study has been retracted and is no longer considered valid scientific evidence.
Summary
This study tested whether hydrogen gas could protect newborn rat brains from injury caused by lack of oxygen. Researchers gave newborn rats hydrogen gas for 30, 60, or 120 minutes after the injury and found that hydrogen treatment reduced the number of dying brain cells in a dose-dependent way (more time = more protection). However, this study has been retracted, meaning the journal removed it from publication, so these results are no longer considered reliable.
Practical Takeaway
Although this retracted rat study suggested hydrogen gas might protect newborn brains from oxygen deprivation injury, the retraction means the findings cannot be trusted. This study cannot inform decisions about hydrogen water use in humans, and much more research—including human trials—would be needed before any therapeutic claims could be made.
Abstract
Hypoxia-ischemia (HI) brain injury is a major cause of neuronal cell death especially apoptosis in the perinatal period. This study was designated to examine the effect of hydrogen therapy on apoptosis in an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 C). Immediately after HI insult, pups were placed into a chamber filled with 2% H(2) for 30 min, 60 min, or 120 min, respectively. 24 h after 2% H2 therapy, the pups were decapitated and brain injury was assessed by 2,3,5-triphenyltetrazoliumchloride (TTC), Nissl, and TUNEL staining, as well as caspase-3, caspase-12 activities in the cortex and hippocampus. H(2) treatment in a duration-dependent manner significantly reduced the number of positive TUNEL cells and suppressed caspase-3 and -12 activities. These results indicated H(2) administration after HI appeared to provide brain protection via inhibition of neuronal apoptosis. (C) 2008 Elsevier Ireland Ltd. All rights reserved.