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Expression of GDNF in spinal cord injury and its repression by ONO-1714

Shojiro Nakashima1, Yukihiro Matsuyama, Yimin Yu

  • 1Department of Orthopaedic Surgery, Nagoya University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya, 466-8550, Japan. shojiro@med.nagoya-u.ac.jp

Neuroreport
|December 25, 2004
PubMed

Insights

The study shows that ONO-1714, an inducible nitric oxide synthase (iNOS) inhibitor, reduces glial cell-line-derived neurotrophic factor (GDNF) and nitric oxide production following spinal cord injury in rats.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Inducible nitric oxide synthase (iNOS) plays a role in spinal cord injury.
  • Glial cell-line-derived neurotrophic factor (GDNF) expression is altered after spinal cord injury.
  • ONO-1714 is a specific inhibitor of iNOS with known neuroprotective effects.

Purpose of the Study:

  • To investigate the effects of ONO-1714 on spinal cord injury.
  • To analyze the expression of GDNF following spinal cord injury in the presence of ONO-1714.

Main Methods:

  • Male Sprague-Dawley rats underwent contusive spinal cord injury.
  • Administration of 0.1 mg/kg ONO-1714 post-injury.
  • Analysis of GDNF mRNA via semi-quantitative RT-PCR.
  • Quantification of GDNF-positive cells using immunohistochemistry.

Main Results:

  • ONO-1714 diminished early-stage GDNF production after spinal cord injury.
  • ONO-1714 reduced nitric oxide production mediated by iNOS.
  • Apoptotic cell count was reduced following ONO-1714 administration.

Conclusions:

  • ONO-1714 impacts GDNF expression and iNOS activity post-spinal cord injury.
  • The findings suggest a potential therapeutic role for ONO-1714 in managing spinal cord injury by modulating inflammatory and neurotrophic responses.

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