Hydrogen Therapy Protects Brain After Traumatic Injury in Mice Study
- Authors
- Fan Wu, Tao Liang, Yang Liu, Yongxing Sun, Baoguo Wang
- Journal
- Experimental Neurology
- Year
- 2024
- DOI
- 10.1016/j.expneurol.2024.114876
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Traumatic Brain Injury
- Body System
- Nervous System
TL;DR
Hydrogen treatment helps protect the brain from injury after a traumatic event by enhancing a cellular cleanup process and reducing cell death.
Key Finding
Hydrogen gas protected brain cells from injury-related damage by triggering a cellular cleanup mechanism involving increased NEDD4 protein and decreased CX43 protein, which together reduced cell death and inflammation.
Summary
Researchers studied how hydrogen gas might protect the brain after traumatic injury in mice. They found that hydrogen treatment activated a cellular cleanup process called mitophagy (where cells remove damaged parts) by increasing a protein called NEDD4 and decreasing another protein called CX43. This process reduced cell death and inflammation in brain cells exposed to injury-mimicking conditions, and hydrogen treatment also improved recovery in injured mice.
Practical Takeaway
This mouse study suggests hydrogen gas may have protective effects on the brain after traumatic injury through a specific cellular mechanism, but this is early-stage research conducted only in animals and cell cultures. Human studies would be needed to determine whether these effects translate to people with traumatic brain injuries.
Abstract
Background: Hydrogen (H2) has emerged as a potential therapeutic intervention for traumatic brain injury (TBI). However, the precise mechanism underlying H2's neuroprotective effects in TBI remain incompletely understood. Methods: TBI mouse model was induced using the controlled cortical impact (CCI) method, and a cell model was established by exposing astrocytes to lipopolysaccharide (LPS). Cell viability was detected by CCK-8 kits. Cell apoptosis was measured by flow cytometry. ELISA was used to detect cytokine quantification. Protein and gene expression was detected by western blot and RT-PCR analysis. Co-immunoprecipitation (CO-IP) were employed for protein-protein interactions. Morris water maze test and rotarod test were applied for TBI mice. Results: H2 treatment effectively inhibited the LPS-induced cell injury and cell apoptosis in astrocytes. NEDD4 expression was increased following HRS treatment coupled with enhanced mitophagy in LPS-treated astrocytes. Overexpression of NEDD4 and down-regulation of connexin 43 (CX43) mirrored the protective effects of H2 treatment in LPS-exposed astrocytes. NEDD4 interacts CX43 to regulates the ubiquitinated degradation of CX43. While overexpression of CX43 reversed the protective effects of H2 treatment in LPS-exposed astrocytes. In addition, H2 treatment significantly alleviated brain injury in TBI mouse model. Conclusion: H2 promoted NEDD4-CX43 mediated mitophagy to protect brain injury induced by TBI, highlighting a novel pathway underlying the therapeutic effects of H2 in TBI.