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Say "no" to spinal cord injury: is nitric oxide an option for therapeutic strategies?

AbstractPURPOSE:
a literature review was made to investigate the role of nitric oxide (NO) in spinal cord injury, a pathological condition that leads to motor, sensory, and autonomic deficit. Besides, we were interested in potential therapeutic strategies interfering with NO mechanism of secondary damage.
MATERIALS:
A literature search using PubMed Medline database has been performed.
RESULTS:
excessive NO production after spinal cord injury promotes oxidative damage perpetuating the injury causing neuronal loss at the injured site and in the surrounding area.
CONCLUSION:
different therapeutic approaches for contrasting or avoiding NO secondary damage have been studied, these include nitric oxide synthase inhibitors, compounds that interfere with inducible NO synthase expression, and molecules working as antioxidant. Further studies are needed to explain the neuroprotective or cytotoxic role of the different isoforms of NO synthase and the other mediators that take part or influence the NO cascade. In this way, it would be possible to find new therapeutic targets and furthermore to extend the experimentation to humans.
AuthorsValentina Tardivo, Emanuela Crobeddu, Giulia Pilloni, Marco Fontanella, Giannantonio Spena, Pier Paolo Panciani, Pedro Berjano, Marco Ajello, Marco Bozzaro, Alessandro Agnoletti, Roberto Altieri, Alessandro Fiumefreddo, Francesco Zenga, Alessandro Ducati, Diego Garbossa
JournalThe International journal of neuroscience (Int J Neurosci) Vol. 125 Issue 2 Pg. 81-90 (Feb 2015) ISSN: 1563-5279 [Electronic] England
PMID24697508 (Publication Type: Journal Article, Review)
Chemical References
  • Enzyme Inhibitors
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
Topics
  • Animals
  • Enzyme Inhibitors (therapeutic use)
  • Humans
  • Nitric Oxide (antagonists & inhibitors, metabolism)
  • Nitric Oxide Synthase Type II (metabolism)
  • PubMed (statistics & numerical data)
  • Spinal Cord Injuries (drug therapy, metabolism)

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