Hydrogen Gas Protects Spinal Cord from Injury in Animal Study
- Authors
- Yi Huang, Keliang Xie, Jipeng Li, Ning Xu, Gu Gong, Guolin Wang, Yonghao Yu, Hailong Dong, Lize Xiong
- Journal
- Brain Research
- Year
- 2011
- DOI
- 10.1016/j.brainres.2010.12.071
- Study Type
- Rabbit
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Spinal Cord Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas helps reduce damage and improve function in rabbit spinal cords after a temporary blood supply cut-off.
Key Finding
Inhaling hydrogen gas at 2% and 4% concentrations significantly reduced spinal cord damage and improved leg function in rabbits after blood flow was blocked and then restored.
Summary
Researchers tested whether inhaling hydrogen gas could protect rabbit spinal cords from damage caused by temporarily cutting off blood flow and then restoring it. They found that rabbits breathing 2% or 4% hydrogen gas showed less nerve damage, better leg movement, and reduced markers of cell damage and inflammation compared to untreated rabbits.
Practical Takeaway
This animal study suggests hydrogen gas inhalation may help protect nerve tissue from ischemia-reperfusion injury, but this research was conducted only in rabbits and would need to be tested in humans before any conclusions could be drawn about its use in medical settings.
Abstract
Recently, hydrogen gas (H₂) is reported to be a new therapeutic agent in organ damage induced by ischemia-reperfusion (I/R). The present study was designed to investigate the beneficial effects of H₂ against spinal cord I/R injury and its associated mechanisms. Spinal cord ischemia was induced by infrarenal aortic occlusion for 20 min in male New Zealand white rabbits. Treatment with 1%, 2% or 4% H₂ inhalation was given from 10 min before reperfusion to 60 min after reperfusion (total 70 min). Here, we found that I/R-challenged animals showed significant spinal cord damage characterized by the decreased numbers of normal motor neurons and hind-limb motor dysfunction, which was significantly improved by 2% and 4 % H₂ treatment. Furthermore, we found that the beneficial effects of H₂ treatment against spinal cord I/R injury were associated with the decreased levels of oxidative products [8-iso-prostaglandin F2α (8-iso-PGF2α) and malondialdehyde (MDA)] and pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1)], as well as increased activities of antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] in serum and spinal cord. In addition, H₂ treatment reduced motor neuron apoptosis in the spinal cord of this model. Thus, H₂ inhalation may be an effective therapeutic strategy for spinal cord I/R damage.