Hydrogen Water Improves Brain Function After Stroke in Mice
- Authors
- Dain Lee, Jong-Il Choi
- Journal
- BioMed Research International
- Year
- 2021
- DOI
- 10.1155/2021/9956938
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- South Korea
- Health Condition
- Stroke
- Body System
- Nervous System
TL;DR
Drinking hydrogen-rich water improved brain health and reduced brain cell death in mice that had a stroke-like condition.
Key Finding
In mice with simulated stroke injury, hydrogen-rich water improved cognitive function and reduced brain cell death while decreasing inflammatory markers and oxidative stress.
Summary
Researchers gave mice with brain injury from blocked blood flow hydrogen-rich water to drink and compared them to untreated mice. The hydrogen-treated mice showed better memory and learning, less brain cell death, and reduced inflammation markers in their brains. The study suggests hydrogen water may protect brain cells from damage caused by stroke-like injuries.
Practical Takeaway
While this mouse study shows promising effects of hydrogen water on brain protection after ischemic injury, it is animal research only and does not demonstrate whether these benefits would occur in humans. Much more research, including human clinical trials, would be needed before hydrogen water could be considered a treatment for stroke or cognitive decline.
Abstract
Background: Cerebral ischemia and its reperfusion injury facilitate serious neurodegenerative diseases such as dementia due to cell death; however, there is currently no treatment for it. Reactive oxygen species is one of the many factors that induce and worsen the development of such diseases, and it can be targeted by hydrogen treatment. This study examined the effect of molecular hydrogen in cerebral ischemia-reperfusion injury, which is emerging as a novel therapeutic agent for various diseases. Methods: Ischemia-reperfusion injury was generated through bilateral common carotid artery occlusion in C57BL/6 mice. The test group received hydrogen-rich water orally during the test period. To confirm model establishment and the effect of hydrogen treatment, behavioural tests, biochemical assays, immunofluorescence microscopy, and cytokine assays were conducted. Results: Open field and novel object recognition tests revealed that the hydrogen-treated group had improved cognitive function and anxiety levels compared to the nontreated group, while hematoxylin and eosin stain showed abundant pyknotic cells in a model mouse brain, and this was attenuated in the hydrogen-treated mouse brain. Total antioxidant capacity and thiobarbituric acid reactive substance assays revealed that hydrogen treatment induced antioxidative effects in the mouse brain. Immunofluorescence microscopy revealed attenuated apoptosis in the striatum, cerebral cortex, and hippocampus of hydrogen-treated mice. Western blotting showed that hydrogen treatment reduced Bax and TNFα levels. Finally, cytokine assays showed that IL-2 and IL-10 levels significantly differed between the hydrogen-treated and nontreated groups. Conclusion: Hydrogen treatment could potentially be a future therapeutic strategy for ischemia and its derived neurodegenerative diseases by improving cognitive abilities and inducing antioxidative and antiapoptotic effects. Hydrogen treatment also decreased Bax and TNFα levels and induced an anti-inflammatory response via regulation of IL-2 and IL-10. These results will serve as a milestone for future studies intended to reveal the mechanism of action of molecular hydrogen in neurodegenerative diseases.