Hydrogen Gas Inhalation Protects Brain Function in Memory Loss Study

Authors
Journal
International Journal of Molecular Sciences
Year
DOI
10.3390/ijms222413313
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
South Korea
Health Condition
Neurodegenerative Diseases
Body System
Nervous System

TL;DR

Breathing in hydrogen gas helped improve memory and reduce signs of brain damage and inflammation in mice that were exposed to a toxin that causes neurodegeneration similar to Alzheimer's disease.

Key Finding

Hydrogen gas inhalation improved memory deficits and reduced oxidative stress markers, inflammation, and Alzheimer's-related proteins in mice with chemically-induced brain damage.

Summary

Researchers exposed mice to a toxic chemical that damages the brain and causes memory problems, then treated some mice by having them breathe hydrogen gas for 30 minutes daily over four weeks. The hydrogen-treated mice showed better memory performance and had lower levels of harmful molecules (like reactive oxygen species) and brain-damaging proteins (like amyloid beta) compared to untreated mice, suggesting hydrogen gas may help protect against cognitive decline.

Practical Takeaway

This mouse study suggests hydrogen gas inhalation may have neuroprotective potential, but it is early-stage research in animals only. Human studies would be needed to determine whether these effects translate to people with cognitive decline or neurodegenerative diseases. The study does not establish whether hydrogen water (a different delivery method) would have similar effects.

Abstract

Oxidative stress (OS) is one of the causative factors in the pathogenesis of various neurodegenerative diseases, including Alzheimer's disease (AD) and cognitive dysfunction. In the present study, we investigated the effects of hydrogen (H2) gas inhalation in trimethyltin (TMT)-induced neurotoxicity and cognitive dysfunction in the C57BL/6 mice. First, mice were divided into the following groups: mice without TMT injection (NC), TMT-only injection group (TMT only), TMT injection + lithium chloride-treated group as a positive control (PC), and TMT injection + 2% H2 inhalation-treated group (H2). The TMT injection groups were administered a single dosage of intraperitoneal TMT injection (2.6 mg/kg body weight) and the H2 group was treated with 2% H2 for 30 min once a day for four weeks. Additionally, a behavioral test was performed with Y-maze to test the cognitive abilities of the mice. Furthermore, multiple OS- and AD-related biomarkers such as reactive oxygen species (ROS), nitric oxide (NO), calcium (Ca2+), malondialdehyde (MDA), glutathione peroxidase (GPx), catalase, inflammatory cytokines, apolipoprotein E (Apo-E), amyloid β (Aβ)-40, phospho-tau (p-tau), Bcl-2, and Bcl-2- associated X (Bax) were investigated in the blood and brain. Our results demonstrated that TMT exposure alters seizure and spatial recognition memory. However, after H2 treatment, memory deficits were ameliorated. H2 treatment also decreased AD-related biomarkers, such as Apo-E, Aβ-40, p-tau, and Bax and OS markers such as ROS, NO, Ca2+, and MDA in both serum and brain. In contrast, catalase and GPx activities were significantly increased in the TMT-only group and decreased after H2 gas treatment in serum and brain. In addition, inflammatory cytokines such as granulocyte colony-stimulating factors (G-CSF), interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α) were found to be significantly decreased after H2 treatment in both serum and brain lysates. In contrast, Bcl-2 and vascular endothelial growth factor (VEGF) expression levels were found to be enhanced after H2 treatment. Taken together, our results demonstrated that 2% H2 gas inhalation in TMT-treated mice exhibits memory enhancing activity and decreases the AD, OS, and inflammatory-related markers. Therefore, H2 might be a candidate for repairing neurodegenerative diseases with cognitive dysfunction. However, further mechanistic studies are needed to fully clarify the effects of H2 inhalation on TMT-induced neurotoxicity and cognitive dysfunction.