Hydrogen Saline Injection Protects Brain Cells After Stroke in Gerbils
- Authors
- Momoko Hirano, Kazuhisa Sugai, Masahiko Fujisawa, Eiji Kobayashi, Yoshinori Katsumata, Yoji Hakamata, Motoaki Sano
- Journal
- PLoS One
- Year
- 2022
- DOI
- 10.1371/journal.pone.0279410
- Study Type
- Gerbil
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Ischemic Stroke
- Body System
- Nervous System
TL;DR
Injecting saline with dissolved hydrogen into the abdomen of gerbils reduced brain cell death after a stroke, even though only a small amount of hydrogen reached the brain.
Key Finding
Intraperitoneal hydrogen-rich saline significantly reduced neuronal cell death in the hippocampus and cortex following stroke in gerbils, despite minimal hydrogen reaching the brain tissue.
Summary
Researchers gave gerbils (small rodents) hydrogen-rich salt water injected into the abdomen after inducing a stroke-like condition. They found that this treatment reduced the death of brain cells in two key brain regions (the hippocampus and cortex) compared to regular salt water. Surprisingly, measurements showed that very little hydrogen actually reached the brain through the bloodstream, suggesting the protective effect may work through an indirect mechanism rather than hydrogen directly protecting brain cells.
Practical Takeaway
This animal study suggests hydrogen may protect against stroke damage through indirect mechanisms in the body rather than direct action in the brain. However, this is early-stage research in gerbils only, and it remains unclear whether these findings would apply to humans or what the practical implications might be for hydrogen water consumption.
Abstract
Intraperitoneal administration of hydrogen (H2)-containing saline inhibited neuronal cell death in ischemic stroke in a number of animal models, but it is unknown whether H2 is absorbed from the abdominal cavity into the blood and reaches the brain. In this study, we investigated whether intraperitoneal administration of saline containing H2 inhibits neuronal cell death caused by cerebral ischemia and measured the concentration of H2 in the carotid artery and inferior vena cava (IVC). Gerbils were subjected to transient unilateral cerebral ischemia twice, and saline or H2-rich saline was administered intraperitoneally three or seven times every 12 hours. We evaluated the number of apoptotic cells in the hippocampus and cerebral cortex on day 3 and the number of viable neurons in the hippocampus and cerebral cortex on day 7. In addition, a single dose of saline or H2-rich saline was administered intraperitoneally, and blood H2 levels in the carotid artery and IVC were measured. On day 3 of ischemia/reperfusion, the number of neurons undergoing apoptosis in the cortex was significantly lower in the H2-rich saline group than in the saline group, and on day 7, the number of viable neurons in the hippocampus and cerebral cortex was significantly higher in the H2-rich saline group. Intraperitoneal administration of H2-rich saline resulted in large increases in H2 concentration in the IVC ranging from 0.00183 mg/L (0.114%) to 0.00725 mg/L (0.453%). In contrast, carotid H2 concentrations remained in the range of 0.00008 mg/L (0.0049%) to 0.00023 (0.0146%). On average, H2 concentrations in carotid artery were 0.04 times lower than in IVC. These results indicate that intraperitoneal administration of H2-rich saline significantly suppresses neuronal cell death after cerebral ischemia, even though H2 hardly reaches the brain.