Hydrogen Water Protects Brain Cells from Stroke-Like Damage
- Authors
- Xiao-Ye Mo, Xiang-Min Li, Chang-Shou She, Xiao-Qin Lu, Cheng-Gen Xiao, Shi-Hai Wang, Guo-Qing Huang
- Journal
- Brain Research
- Year
- 2019
- DOI
- 10.1016/j.brainres.2018.09.037
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Stroke
- Body System
- Nervous System
TL;DR
Hydrogen-rich saline helps protect nerve cells from damage caused by oxygen and glucose deprivation followed by reperfusion, a process similar to what happens during a stroke.
Key Finding
Hydrogen-rich saline protected rat nerve cells from oxygen and glucose deprivation damage by increasing Bcl-2 protein levels, which suppressed a mitochondrial channel (VDAC1) and prevented cell death.
Summary
Researchers tested hydrogen-rich saline on rat nerve cells in a laboratory dish to understand how it might protect cells from damage caused by lack of oxygen and glucose (a condition similar to stroke). They found that hydrogen-rich saline increased production of a protective protein called Bcl-2, which prevented cells from dying through a process called apoptosis (programmed cell death). The treatment appeared to work by blocking a channel in the cell's energy-producing structures (mitochondria) that would normally release harmful substances.
Practical Takeaway
This laboratory study in rat cells suggests hydrogen-rich saline may have protective effects against ischemic (oxygen-deprived) cell damage, but it is very early-stage research. The findings are limited to cells grown in a dish and have not been tested in animals or humans, so it is not yet clear whether these results would translate to actual health benefits.
Abstract
Background: Hydrogen is received as an inert gas that thought to be non-functional in vivo previously. Recently, emerging evidences showed that in ischemia/reperfusion (IR) condition, hydrogen reduced cellular reactive oxygen species (ROS) production and ameliorated cell apoptosis. However, the underlying mechanism of hydrogen on IR-induced apoptosis remains elusive. Here we tried to unravel the mode of action of hydrogen with rat adrenal medulla cell line PC-12 in vitro. Methods: The mitochondrial functions before and after oxygen glucose deprivation and reperfusion (OGD/RP) were determined with corresponding dyes. The expression of Bcl-2, Bax, VDAC1, cytochrome c and caspase 9 was detected using qRT-PCR and Western Blotting method. Then Bcl-2 inhibitor, AB-199, was applied to investigate the role of Bcl-2 in OGD/RP-induced cell apoptosis. Finally, we manipulated the expression of VDAC1 with plasmids transfection to understand the effects of VDAC1 on Bcl-2-mediated anti-apoptosis in OGD/RP. Results: In this study, we demonstrated that hydrogen-rich saline (HRS) reduced OGD/RP-mediated neuronal loss by stimulating the expression of Bcl-2, which suppressed the activity of VDAC1. Consequently, HRS maintained the mitochondrial functions, restrained the release of cytochrome c and caspase 9 activation, resulting in ameliorated cell viability. Conclusions: HRS ameliorated OGD/RP-induced PC-12 cell apoptosis and provided a novel treatment option for ischemia.