PURPOSE: 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.
PURPOSE: 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.
Authors: R Altieri; M Fontanella; A Agnoletti; P P Panciani; G Spena; E Crobeddu; G Pilloni; V Tardivo; M Lanotte; F Zenga; A Ducati; D Garbossa Journal: Transl Med UniSa Date: 2014-09-01
Authors: Alexandra Boyko; Alexander Ksenofontov; Sergey Ryabov; Lyudmila Baratova; Anastasia Graf; Victoria Bunik Journal: Front Med (Lausanne) Date: 2018-01-15