Cyclosporin-A inhibits inducible nitric oxide synthase activity and expression after spinal cord injury in rats

Neurosci Lett. 2004 Feb 26;357(1):49-52. doi: 10.1016/j.neulet.2003.12.042.

Abstract

Nitric oxide is generated from l-arginine by a family of three distinct nitric oxide synthase (NOS) enzymes playing a crucial role in the physiopathology of spinal cord injury (SCI). Cyclosporin-A (CsA), an immunosupressive agent, may be used to inhibit the activity of iNOS and perhaps to protect against neural tissue destruction. Rats were submitted to SCI by contusion, and killed 4, 24 and 72 h after lesion. Results showed an increase in the activity of iNOS at 72 h after the SCI, inhibited by CsA (2.5 mg/kg) administered 12 h after trauma. iNOS Western blot assay showed an increase in the expression of iNOS after trauma, also antagonized by CsA administration.

MeSH terms

  • Animals
  • Cyclosporine / pharmacology*
  • Disease Models, Animal
  • Female
  • I-kappa B Proteins / drug effects
  • I-kappa B Proteins / metabolism
  • Immunosuppressive Agents / pharmacology
  • NF-kappa B / drug effects
  • NF-kappa B / metabolism
  • Nerve Degeneration / drug therapy*
  • Nerve Degeneration / enzymology
  • Nerve Degeneration / prevention & control*
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Rats
  • Rats, Wistar
  • Spinal Cord Injuries / drug therapy*
  • Spinal Cord Injuries / enzymology
  • Spinal Cord Injuries / physiopathology
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / physiology

Substances

  • I-kappa B Proteins
  • Immunosuppressive Agents
  • NF-kappa B
  • Nitric Oxide
  • Cyclosporine
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat