Hydrogen Gas Protects Brain After Stroke in Animal Study
- Authors
- Kyu-Sun Choi, Han-Jun Kim, Sun Hee Do, Se Jin Hwang, Hyeong-Joong Yi
- Journal
- Brain Research Bulletin
- Year
- 2018
- DOI
- 10.1016/j.brainresbull.2018.07.006
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- South Korea
- Health Condition
- Intracerebral Hemorrhage
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas helped protect rat brains from damage and inflammation after a stroke-like injury.
Key Finding
Hydrogen gas inhalation reduced oxidative stress, inflammation, and cell death in rats with experimentally induced brain bleeding, with the strongest protective effects observed within 24 hours of treatment.
Summary
Researchers gave rats a brain injury similar to a stroke caused by bleeding, then treated some with inhaled hydrogen gas. The hydrogen-treated rats showed less brain swelling, better neurological function, and reduced markers of cell damage and inflammation compared to untreated injured rats. The protective effects were strongest when measured within 24 hours of treatment.
Practical Takeaway
While this rat study suggests hydrogen inhalation may protect brain tissue after bleeding injuries through multiple mechanisms, these results cannot yet be applied to humans. Further research in human subjects would be needed to determine whether hydrogen therapy could help stroke patients, and the optimal timing and dosage remain unknown.
Abstract
Objective: Hydrogen inhalation has been found to be neuroprotective and anti-oxidative in several brain injury models. Building on these studies, we investigated potential neuroprotective effects of hydrogen inhalation in a rat model of intracerebral hemorrhage (ICH), focusing on apoptosis and inflammation. Methods: Forty-five 8-week-old male Sprague-Dawley rats were randomly divided into three groups (n = 15 per each group): a sham group, ICH group, and ICH + hydrogen group. Induction of ICH was performed via injection of 0.23 U of bacterial collagenase type IV into the left striatum. Hydrogen was administered via spontaneous inhalation. Mortality and neurologic deficits were investigated at 6, 24, and 48 hours after ICH. To investigate the antioxidative activity of hydrogen gas, the expression of malondialdehyde was measured. Real-time polymerase chain reaction analyses of TNF-a, IL-1b, BDNF, and caspase-3 expression were used to detect anti-inflammatory and anti-apoptotic effects. Neuroprotective effect was evaluated by immunohistochemical and TUNEL staining. Result: At 6, 24 and 48 hours post-intracerebral hemorrhage, animals showed brain edema and neurologic deficits, accompanied by up-regulation of TNF-a, IL-b, BDNF, and caspase-3, which is indicative of neuroinflammation, neuroprotection, and apoptosis. Hydrogen treatment significantly reduced the level of oxidative stress, neuroinflammation, neuronal damage, and apoptosis-related genes. This was accompanied by increased neurogenesis and expression of growth factor-related genes at <24 hours, but not 48 hours, after ICH. Conclusion: H2 gas administration exerted a neuroprotective effect against early brain injury after ICH through anti-inflammatory, neuroprotective, anti-apoptotic, and antioxidative activity.