Hydrogen Gas Protects Brain Cells After Stroke in Rats
- Authors
- Marietta Hugyecz, Éva Mracskó, Péter Hertelendy, Eszter Farkas, Ferenc Domoki, Ferenc Bari
- Journal
- Brain Research
- Year
- 2011
- DOI
- 10.1016/j.brainres.2011.05.068
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Hungary
- Health Condition
- Stroke
- Body System
- Nervous System
TL;DR
Breathing in air with added hydrogen gas may help protect the brain from damage after a temporary loss of blood flow and oxygen.
Key Finding
Hydrogen-enriched air inhalation prevented increases in inflammatory enzymes and maintained normal levels of gap junction proteins in rat brains after temporary oxygen deprivation, matching the protective effects of rosiglitazone.
Summary
This rat study examined whether breathing air enriched with hydrogen gas could protect the brain after a temporary loss of blood flow and oxygen (a type of stroke). Researchers found that hydrogen-enriched air inhalation prevented harmful changes in brain proteins and inflammation markers in the hippocampus (a memory-related brain region) three days after the injury, performing similarly to a comparison drug called rosiglitazone.
Practical Takeaway
This early animal evidence suggests hydrogen gas inhalation may have neuroprotective potential for brain injury from stroke, but this is a rat study only and much more research—including human trials—would be needed before any conclusions about human benefit. The lack of reported side effects in this model is encouraging, but safety and effectiveness in people remain unknown.
Abstract
Transient global cerebral ischemia (TGCI) occurs during acute severe hypotension depriving the brain of oxygen and glucose for a short period of time. During reperfusion, several mechanisms can induce secondary neuronal damage, including the increased production of reactive oxygen species (ROS). Hydrogen gas-enriched air inhalation is a neuroprotective approach with proven antioxidant potential, which has not yet been examined in TGCI. Accordingly, we set out to describe the effect of inhalation of 2.1% hydrogen supplemented room air (H(2)-RA) in comparison with a well studied neuroprotective agent, rosiglitazone (RSG) in a TGCI rat model. Male Wistar rats were exposed to TGCI (n=26) or sham operation (n=26), while a third group served as intact control (naive, n=5). The operated groups were further divided into non-treated, H(2)-RA, RSG (6 mg/kg i.v.) and vehicle treated animals. Tissue samples from the hippocampus and frontal cortex were taken 3 days following surgery. Western blot analysis was applied to determine the expressions of cyclooxygenase-2 (COX-2), neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively), manganese superoxide dismutase (MnSOD) and glial connexin proteins: connexin 30 and connexin 43. The expressions of COX-2, and connexin proteins were upregulated, while nNOS was downregulated 3 days after TGCI. Both RSG and H(2)-RA prevented the changes of enzyme and connexin levels. Considering the lack of harmful side effects, inhalation of H(2)-RA can be a promising approach to reduce neuronal damage after TGCI.