Hydrogen Water Protects Brain Cells in Parkinson's Through Multiple Pathways
- Authors
- Yusuke Yoshii, Taikai Inoue, Yuya Uemura, Yusaku Iwasaki, Toshihiko Yada, Yusaku Nakabeppu, Mami Noda
- Journal
- Neurochemical Research
- Year
- 2017
- DOI
- 10.1007/s11064-017-2281-1
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Parkinson's Disease
- Body System
- Nervous System
TL;DR
Drinking hydrogen-rich water may protect the brain in Parkinson's disease through mechanisms other than the stomach hormone ghrelin, as shown by experiments in mice.
Key Finding
Molecular hydrogen's protective effects in Parkinson's disease models do not depend solely on ghrelin signaling or vagal nerve communication, indicating multiple biological pathways are involved.
Summary
Researchers studied how molecular hydrogen (H2)—a gas dissolved in drinking water—might protect brain cells in mice with Parkinson's disease. They initially thought H2 worked by triggering a stomach hormone called ghrelin, which sends signals to the brain through the vagus nerve (a major nerve connecting stomach and brain). However, when they tested mice without ghrelin or with severed vagus nerves, H2 water still provided protection, suggesting the mechanism is more complex than previously thought.
Practical Takeaway
This is an early-stage animal study that suggests H2 water's effects in Parkinson's disease may work through multiple mechanisms, not just one pathway. However, these findings are from mice only and do not yet translate to human applications or health recommendations. More research is needed to identify what other factors enable H2's protective effects and whether similar mechanisms occur in people.
Abstract
Molecular hydrogen (H2), as a new medical gas, has protective effects in neurological disorders including Parkinson's disease (PD). In our previous report, the neuroprotective effect of drinking water with saturated H2 (H2 water) in PD mice might be due to stomach-brain interaction via release of gastric hormone, ghrelin. In the present study, we assessed the effect of H2-induced ghrelin more precisely. To confirm the contribution of ghrelin in H2 water-drinking PD model mice, ghrelin-knock out (KO) mice were used. Despite the speculation, the effect of H2 water was still observed in ghrelin-KO PD model mice. To further check the involvement of ghrelin, possible contribution of ghrelin-induced vagal afferent effect was tested by performing subdiaphragmatic vagotomy before treating with H2 water and administration of MPTP (1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine). The protective effect of H2 water was still observed in the vagotomized mice in substantia nigra, suggesting that stimulation of vagal afferent nerves is not involved in H2-induced neuroprotection. Other neuroprotective substitutes in ghrelin-KO mice were speculated because H2-induced neuroprotection was not cancelled by ghrelin receptor antagonist, D-Lys3 GHRP-6, in ghrelin-KO PD model mice, unlike in wild-type PD model mice. Our results indicate that ghrelin may not be the only factor for H2-induced neuroprotection and other factors can substitute the role of ghrelin when ghrelin is absent, raising intriguing options of research for H2-responsive factors.