Hydrogen Gas Inhalation Helps Heal Spinal Cord Injuries in Mice
- Authors
- Xiao Chen, Jin Cui, Xiao Zhai, Jun Zhang, Zhengrong Gu, Xin Zhi, Weizong Weng, Panpan Pan, Liehu Cao, Fang Ji, Zhiwei Wang, Jiacan Su
- Journal
- Cellular Physiology and Biochemistry
- Year
- 2018
- DOI
- 10.1159/000489764
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Spinal Cord Injury
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas can help reduce damage and improve recovery in mice with spinal cord injuries by targeting harmful molecules and preserving nerve cell health.
Key Finding
Hydrogen gas inhalation at 75% concentration reduced nerve cell death, decreased harmful oxidative damage, and preserved mitochondrial function in mice with spinal cord injuries, leading to improved movement and walking ability.
Summary
Researchers tested whether breathing hydrogen gas could help repair spinal cord injuries in mice. They found that hydrogen gas reduced damage to nerve cells by decreasing harmful molecules called reactive oxygen species, preventing cell death, and protecting the energy-producing structures inside cells called mitochondria. Mice that breathed hydrogen gas showed improved movement and walking ability after spinal cord injury compared to untreated mice.
Practical Takeaway
This study provides early evidence that hydrogen gas may protect nerve cells from injury-related damage in spinal cord trauma, but it was conducted only in mice. Much more research, including human trials, would be needed before hydrogen therapy could be considered a treatment option for spinal cord injury in people.
Abstract
Background/aims: Hydrogen selectively neutralizes reactive oxygen species (ROS) and ameliorates various ROS-induced injuries. Spinal cord injury (SCI) is a serious injury to the central nervous system, and secondary SCI is closely related to excessive ROS generation. We hypothesized that hydrogen inhalation ameliorates SCI, and the mechanism of action may be related to the protective effects of hydrogen against oxidative stress, apoptosis, and mitochondrial damage. Methods: Mechanically injured spinal cord neurons were incubated with different concentrations of hydrogen in vitro. Immunofluorescence staining and transmission electron microscopy were used to confirm the protective effects of hydrogen. ROS and related proteins were detected with dihydroethidium fluorescence staining, enzyme-linked immunosorbent assays, and western blotting. Terminal deoxynucleotidyl transferase dUTP nick end labeling assays, flow cytometry, and western blotting were used to detect neuronal apoptosis. ATP concentrations, Janus Green B staining, and mitochondrial permeability transition pore (mPTP) status were assessed to investigate mitochondrial damage. RNA sequencing was performed to screen potential target genes of hydrogen application. Hydrogen was administered to mice after spinal cord contusion injury was established for 42 days. The Basso Mouse Scale (BMS) and footprint analyses were used to assess locomotor functions, and immunofluorescence staining of the injured spinal cord segments was performed to detect oxidative stress status. Results: Spinal cord neurons were preserved by hydrogen administration after mechanical injury in a dose-dependent manner. ROS generation, oxidative stress injury-related markers, and the number of apoptotic neurons were significantly reduced after hydrogen treatment. The ATP production and mPTP function in injured neurons were preserved by hydrogen incubation. The expression levels of Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were inhibited by hydrogen treatment. BMS scores and the footprint assessment of mice with SCI were improved by hydrogen inhalation. Conclusions: Hydrogen inhalation (75%) ameliorated SCI in vivo and attenuated neuronal mechanical injuries in vitro, and its protective effect on spinal cord neurons was exerted in a dose-dependent manner. The underlying mechanisms included reducing ROS generation and oxidative stress, inhibiting neuronal apoptosis, and restoring mitochondrial construction and function. Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were identified as potential target genes of hydrogen treatment.