Can hydrogen water protect brain cells from damage?

Yes, this study found that hydrogen-rich water significantly protected mouse brain cells from oxidative stress damage. The protection worked by activating cellular survival pathways that enhance the brain's natural antioxidant defenses.

How does hydrogen water protect brain cells?

Hydrogen water activates the PI3K/Akt signaling pathway in brain cells, which controls cell survival and antioxidant responses. When this pathway was blocked in the study, the protective effects completely disappeared.

What concentration of hydrogen water was most effective?

The researchers found that 50 micromoles per liter of hydrogen water, applied for 9 hours before oxidative damage, provided the best protection for brain cells. Higher or lower concentrations were less effective.

Could hydrogen water help with brain diseases?

This laboratory study suggests hydrogen water might help conditions involving brain cell damage from oxidative stress, like stroke or neurodegenerative diseases. However, human clinical trials are needed to confirm these potential benefits.

Is hydrogen water treatment safe for brain cells?

In this study, hydrogen water showed no toxic effects on brain cells at therapeutic concentrations. The treatment actually improved cell survival and activated protective pathways without causing harm.

Hydrogen Water Protects Brain Cells from Oxidative Damage

Authors: Ruiting Lu, Yadi Liu, Difen Wang
Journal: Chinese Critical Care Medicine
Year: 2019
DOI: 10.3760/cma.j.issn.2095-4352.2019.06.020
Study Type: Cell Culture
Outcome: Positive
Peer Reviewed: Yes
Country: China
Health Condition: Oxidative Stress
Body System: Nervous System

TL;DR

Drinking hydrogen-rich water may help protect brain cells from oxidative damage by activating a cell-survival signaling pathway.

Key Finding

Hydrogen-rich water protected lab-grown mouse brain cells from oxidative stress damage by activating the PI3K/Akt cellular pathway, and blocking this pathway eliminated the protective effect.

Summary

Researchers grew mouse brain cells in a lab and exposed them to hydrogen peroxide to simulate oxidative stress (cellular damage from harmful molecules). They then treated some cells with hydrogen-rich water and found it protected the cells from damage by activating a specific cellular pathway called PI3K/Akt, which helps cells defend themselves. When they blocked this pathway with a chemical inhibitor, the protective effect disappeared, suggesting this pathway is essential for hydrogen-rich water's protective action.

Practical Takeaway

This is an early-stage laboratory study using cultured cells, not living organisms or humans, so results cannot yet be applied to health claims. The findings suggest a potential mechanism by which hydrogen-rich water might protect brain cells from oxidative damage, but much more research—including animal and human studies—would be needed to determine if this translates to real-world benefits.

Abstract

Objective: To explore the protective effect of hydrogen-rich water on the oxidative stress injury of astrocytes in mice and its effect on phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signal pathway. Methods: In vitro, mice astrocytes were cultured and the logarithmic growth period cells were taken for experiment. (1) Experiment one: some cells were acted by 1.25, 2.50, 5.00, 10.00 μmol/L hydrogen peroxide (H2O2) for 20 minutes to determine the appropriate concentration required for astrocyte damage induced by H2O2; cultivating 3, 6, 9, and 12 hours with hydrogen-rich water of 25, 50, 100, and 200 μmol/L, respectively, to determine the concentration and time of hydrogen-rich water pretreatment; the 50 μmol/L hydrogen-rich water was cultured together with PI3K/Akt signal pathway inhibitors wortmannin (WM) 200 nmol/L or 400 nmol/L to determine the best inhibition concentration of wortmannin. Astrocyte activity was detected by methyl thiazolyl tetrazolium (MTT) colorimetry. (2) Experiment two: some cells were divided into blank control group, H2O2 injury group, hydrogen-rich water pretreatment group (HW+H2O2 group), and co-culture of hydrogen-rich water and wortmannin pretreatment group (HW+WM+H2O2 group). The mRNA expressions of PI3K and Akt were detected by reverse transcription-polymerase chain reaction (RT-PCR); the protein expressions of PI3K, Akt and phosphorylated Akt (p-Akt) were detected by Western Blot. Results: (1) Experiment one: the survival rate of the blank control group was 100%. Cell activity gradually decreased with the increase of H2O2 concentration, and the survival rate of the H2O2 action 20 minutes cells of 2.50 μmol/L was reduced to about 50%, so a cell injury model was established at this concentration. With the increase of hydrogen-rich water pretreatment concentration, and the duration of action, the cell survival rate increased first and then decreased. The cell survival rate was highest when 50 μmol/L hydrogen-rich water was pretreated with 9 hours, so a hydrogen-rich water pre-protection model was established. After 200 nmol/L or 400 nmol/L wortmannin was cultured together with hydrogen-rich water, cell activity was inhibited, and the cell survival rate of 200 nmol/L wortmannin group was no significantly different compared with that of H2O2 injury group, so the astrocyte suppression model was established. (2) Experiment two: compared with the blank control group, the mRNA expressions of PI3K and Akt and the protein expressions of PI3K, Akt and p-Akt were significantly decreased in the H2O2 injury group. Compared with the H2O2 injury group, the PI3K, Akt mRNA expressions and PI3K, Akt, p-Akt protein expressions were significantly increased in the HW+H2O2 group [PI3K mRNA (2-ΔΔCT): 0.843±0.019 vs. 0.631±0.038, Akt mRNA (2-ΔΔCT): 0.591±0.025 vs. 0.558±0.037, PI3K/β-actin: 1.277±0.008 vs. 0.757±0.004, Akt/β-actin: 1.308±0.015 vs. 0.682±0.006, p-Akt/β-actin: 1.210±0.005 vs. 0.614±0.005, all P 0.05). Conclusions: Hydrogen-rich water activates the PI3K/Akt pathway, thereby mediates mice astrocytes to exert the biological function of antioxidant.