Hydrogen-rich saline protects against spinal cord injury in rats

Chengwen Chen, Qianbo Chen, Yanfei Mao, Shengming Xu, Chunyan Xia, Xueyin Shi, John H. Zhang, Hongbin Yuan, Xuejun Sun

Research output: Contribution to journalArticlepeer-review

Abstract

In the present study, we examined the mechanisms of hydrogen-rich saline, a reported therapeutic antioxidant, in the treatment of acute spinal cord contusion injury. Male Sprague-Dawley rats were used to produce a standardized model of contuses spinal cord injury (125 kdyn force). Hydrogen-rich saline was injected intraperitoneally (5 ml/kg) immediately, and at 24 and 48 h after injury. All rats were sacrificed at 72 h after spinal cord injury (SCI). Apoptotic cell death, oxidative stress, inflammation, level of Brain derived neurotrophic factor (BDNF) were evaluated. In addition, locomotor behavior was assessed using the Basso, Beattice and Bresnahan (BBB) scale. We observed that administration of hydrogen-rich saline decreased the number of apoptotic cells, suppressed oxidative stress, and improved locomotor functions. Hydrogen-rich saline increased the release of BDNF. In conclusion, hydrogen-rich saline reduced acute spinal cord contusion injury, possibly by reduction of oxidative stress and elevation of BDNF. © 2010 Springer Science+Business Media, LLC.
Original languageEnglish
Pages (from-to)1111-1118
Number of pages8
JournalNeurochemical Research
Volume35
Issue number7
DOIs
StatePublished - Jul 2010

ASJC Scopus Subject Areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Keywords

  • BDNF
  • Hydrogen-rich saline
  • Neuroprotection
  • Oxidative free radicals
  • Spinal cord injury
  • Antioxidants/therapeutic use
  • Protein Carbonylation
  • Malondialdehyde/metabolism
  • Oxidative Stress
  • Rats
  • Spinal Cord/metabolism
  • Hindlimb/physiopathology
  • Male
  • Spinal Cord Injuries/metabolism
  • Rats, Sprague-Dawley
  • Caspases/metabolism
  • Brain-Derived Neurotrophic Factor/metabolism
  • Animals
  • Sodium Chloride/therapeutic use
  • Cell Death
  • Hydrogen/therapeutic use
  • Peroxidase/metabolism
  • Apoptosis

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