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Beneficial effects of hydrogen gas against spinal cord ischemia–reperfusion injury in rabbits
 
 

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 F2 (8-iso-PGF2) and malondialdehyde (MDA)] and pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-) 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.

Research Highlights

► H2 treatment attenuated spinal cord ischemia–reperfusion injury. ► H2 treatment reduced the levels of oxidative products in serum and spinal cord. ► H2 treatment upregulated the activities of antioxidant enzymes. ►H 2 treatment decreased the levels of pro-inflammatory cytokines. ► H2 treatment significantly reduced motor neuron apoptosis of spinal cord.

Abbreviations

  • CAT, catalase;
  • HMGB1, high-mobility group box 1;
  • H2, hydrogen gas;
  • I/R, ischemia–reperfusion;
  • 8-iso-PGF2, 8-iso-prostaglandin F2;
  • MDA, malondialdehyde;
  • ROS, reactive oxygen species;
  • SOD, superoxide dismutase;
  • TNF-, tumor necrosis factor-alpha, TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling

14-04-11 02:34
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