Hydrogen Saline Protects Newborn Brains from Oxygen Loss Damage
- Authors
- Jianmei Cai, Zhimin Kang, Kan Liu, WenWu Liu, RunPing Li, John H. Zhang, Xu Luo, Xue-Jun Sun
- Journal
- Brain Research
- Year
- 2008
- DOI
- 10.1016/j.brainres.2008.11.048
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Neonatal Hypoxia-Ischemia
- Body System
- Nervous System
TL;DR
Treating newborn rats with hydrogen-enriched saline shortly after a brain injury reduces brain damage and improves long-term brain function.
Key Finding
Hydrogen saline treatment reduced brain damage markers and improved long-term neurological function in newborn rats exposed to oxygen and blood flow deprivation.
Summary
Researchers tested whether hydrogen-infused saline could protect newborn rat brains from damage caused by lack of oxygen and blood flow. Young rats were given oxygen deprivation to mimic birth complications, then treated with hydrogen saline injections. The treatment reduced brain cell death, inflammation, and damage markers, and the treated rats showed better brain function and learning ability five weeks later.
Practical Takeaway
This early-stage animal study suggests hydrogen saline may have protective effects against brain injury from oxygen deprivation in newborns, but these results are from rats only and much more research—including human trials—would be needed before any clinical use. The findings are preliminary and cannot yet inform real-world medical decisions.
Abstract
Cerebral hypoxia-ischemia (HI) represents a major cause of brain damage in the term newborn. This study aimed to examine the short and long-term neuroprotective effect of hydrogen saline (H(2) saline) using 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 degrees C). H(2) saturated saline was administered by peritoneal injection (5 ml/kg) immediately and again at 8 h after HI insult. At 24 h after HI, the pups were decapitated and brain morphological injury was assessed by 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, and TUNEL staining. Acute cell death, inflammation and oxidative stress were evaluated at 24 h by studying caspase-3 activity, MDA measurement as well as Iba-1 immunochemistry in the brain. At 5 weeks after HI, spontaneous activity test and Morris water maze test were conducted. We observed that H(2) saline treatment reduced the caspase activity, MDA, Iba-1 levels, the infarct ratio, and improved the long-term neurological and neurobehavioral functions. H(2) saline has potentials in the clinical treatment of HI and other ischemia-related cerebral diseases.