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Related Experiment Videos

Mn-SOD and Bcl-2 expression after repeated hyperbaric oxygenation.

K Wada1, T Miyazawa, N Nomura

  • 1Department of Neurosurgery, National Defense Medical College, Saitama, Japan.

Acta Neurochirurgica. Supplement
|July 14, 2001
PubMed
Summary

Repeated hyperbaric oxygen (HBO) pretreatment, specifically five sessions at 2 ATA, enhances ischemic tolerance by increasing Bcl-2 and Mn-SOD (manganese-superoxide dismutase) in gerbil hippocampus. This suggests a protective mechanism involving these proteins.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Ischemic stroke causes significant neuronal damage.
  • Hyperbaric oxygen (HBO) therapy has shown potential in inducing ischemic tolerance.
  • The underlying mechanisms of HBO-induced neuroprotection require further elucidation.

Purpose of the Study:

  • To investigate the effect of repeated hyperbaric oxygen (HBO) pretreatment on apoptosis-regulating proteins (Bcl-2 and Bax) and manganese-superoxide dismutase (Mn-SOD) in the gerbil hippocampus.
  • To determine the specific HBO treatment parameters that confer ischemic tolerance.

Main Methods:

  • Gerbils were subjected to different HBO pretreatment regimens (e.g., 5 sessions at 2 ATA every other day, 10 sessions at 3 ATA daily) or sham pretreatment.
  • Immunoreactivity for Bcl-2, Bax, and Mn-SOD in the CA1 hippocampal sector was assessed.

Related Experiment Videos

  • Neuronal density in the CA1 hippocampal neurons was evaluated.

    • Main Results:

    • Five sessions of HBO at 2 ATA every other day significantly increased Bcl-2 and Mn-SOD immunoreactivity in the CA1 sector compared to sham pretreatment.
    • Ten daily sessions of HBO at 3 ATA did not yield the same significant increases.
    • No significant differences in Bax immunoreactivity or neuronal density were observed between groups.

    Conclusions:

    • Repeated HBO pretreatment, under specific conditions (5 sessions at 2 ATA), enhances ischemic tolerance in gerbils.
    • The observed neuroprotection is likely mediated by increased expression of Bcl-2 and Mn-SOD, suggesting a role in preventing mitochondrial alterations post-ischemia.