Hydrogen Gas Helps Brain Recovery After Stroke in Rats
- Authors
- Jing-Hua Song, Hong-Yan Jia, Tian-Peng Shao, Zhi-Bao Liu, Yuan-Ping Zhao
- Journal
- Experimental and Therapeutic Medicine
- Year
- 2021
- DOI
- 10.3892/etm.2021.10555
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas reduces brain damage and improves memory and behavior in rats after a brain hemorrhage by blocking harmful cell signals.
Key Finding
Hydrogen gas inhalation reduced brain cell death, improved memory, and decreased anxiety-like behavior in rats recovering from a simulated subarachnoid hemorrhage.
Summary
Researchers gave rats a brain injury similar to a type of stroke called subarachnoid hemorrhage, then treated some rats by having them breathe hydrogen gas for 2 hours. Compared to untreated rats, the hydrogen-treated rats showed less brain cell death, better memory, and less anxiety-like behavior 30 days after the injury. The researchers believe hydrogen gas may work by blocking a specific cell damage pathway in the brain.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas may have protective effects on the brain after certain types of injury. However, these results are from rats only and have not been tested in humans, so it's unclear whether the same benefits would apply to people. Much more research would be needed before hydrogen gas could be considered a treatment for stroke or brain injury in humans.
Abstract
Subarachnoid hemorrhage (SAH) results in high rates of mortality and lasting disability. Hydrogen gas (H2) is an antioxidant with demonstrated neuroprotective efficacy. The present study examined the therapeutic efficacy of H2 inhalation on early brain injury following experimental SAH in rats and the potential underlying molecular mechanisms. The rats were randomly separated into three groups (n=36 per group): Sham, SAH and SAH + H2. Endovascular perforation of the right internal carotid artery was used to establish SAH. After perforation, rats in the SAH + H2 group inhaled 2.9% H2 with regular oxygen for 2 h. Then, 24 h post-SAH, TUNEL staining was used to detect apoptotic neurons, and both immunostaining and western blotting were conducted to examine changes in p38 MAPK activity and the expression levels of apoptotic regulators (Bcl-2, Bax and cleaved caspase-3) in the ventromedial prefrontal cortex. Then, 30 day post-SAH, Nissl staining was performed to detect neuronal injury, brain MRI was conducted to detect gross changes in brain structure and metabolism, the open field test was used to assess anxiety and the novel object recognition test was performed to assess memory. H2 inhalation following experimental SAH stabilized brain metabolites, improved recognition memory and reduced anxiety-like behavior, the neuronal apoptosis rate, phosphorylated p38 MAPK expression, cleaved caspase-3 expression and the Bax/Bcl-2 ratio. Collectively, the present results suggested that H2 inhalation can alleviate SAH-induced cognitive impairment, behavioral abnormalities and neuronal apoptosis in rats, possibly via inhibition of the p38 MAPK signal pathway.