TY - JOUR
T1 - Say "no" to spinal cord injury
T2 - Is nitric oxide an option for therapeutic strategies
AU - Tardivo, Valentina
AU - Crobeddu, Emanuela
AU - Pilloni, Giulia
AU - Fontanella, Marco
AU - Spena, Giannantonio
AU - Panciani, Pier Paolo
AU - Berjano, Pedro
AU - Ajello, Marco
AU - Bozzaro, Marco
AU - Agnoletti, Alessandro
AU - Altieri, Roberto
AU - Fiumefreddo, Alessandro
AU - Zenga, Francesco
AU - Ducati, Alessandro
AU - Garbossa, Diego
PY - 2015/2/1
Y1 - 2015/2/1
N2 - 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.
AB - 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.
KW - Inducible nitric oxide synthase
KW - Nitric oxide
KW - Spinal cord injury
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U2 - 10.3109/00207454.2014.908877
DO - 10.3109/00207454.2014.908877
M3 - Article
C2 - 24697508
AN - SCOPUS:84919625754
VL - 125
SP - 81
EP - 90
JO - International Journal of Neuroscience
JF - International Journal of Neuroscience
SN - 0020-7454
IS - 2
ER -