Modulation of nitric oxide homeostasis in a mouse model of spinal cord injury

2006 ◽  
Vol 4 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Tiziana Genovese ◽  
Emanuela Mazzon ◽  
Sofia Mariotto ◽  
Marta Menegazzi ◽  
Salvatore Cardali ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neutrophil Infiltration ◽  
Adenosine Diphosphate ◽  
Spinal Cord Tissue ◽  
Secondary Damage ◽  
Cord Injury ◽  
Primary Damage ◽  
Oxide Synthase

Object A traumatic spinal cord injury (SCI) immediately induces primary damage, and this is followed by secondary damage characterized by a series of events among which is a progressive extension of cell death within the damaged tissue. In this study, the authors investigated the role of inducible nitric oxide synthase (iNOS) in an experimental model of SCI in mice. Methods In wild-type (iNOS+/+) mice, SCI rapidly induced an inflammatory response as shown by nitrotyrosine formation, activation of the nuclear enzyme poly(adenosine diphosphate-ribose) polymerase (PARP), neutrophil infiltration, and spinal cord tissue histopathological changes, indicating the involvement of iNOS-derived massive amounts of NO in SCI. Conclusions Genetic inhibition of iNOS, however, resulted in a significant reduction in secondary damage, and this therapeutic efficacy was associated with the prevention of an SCI-induced drop in neuronal and endothelial NOS activity.

Effect of anti—rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5′-triphosphatase and superoxide dismutase activation, and ultrastructural changes

2001 ◽  
Vol 95 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Metin Tuna ◽  
Sait Polat ◽  
Tahsin Erman ◽  
Faruk Ildan ◽  
A. Iskender Göçer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Tissue ◽  
Inos Activity ◽  
Content Type ◽  
Cord Injury ◽  
Oxide Synthase ◽  
Fine Print ◽  
Inducible Nitric Oxide

Object. The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti—rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5′-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. Methods. Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2–7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 µg) intraperitoneal injection of anti—rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. Conclusions. The results showed that neutralizing IL-6 bioactivity with anti—rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

Beneficial effects of nitric oxide synthase inhibition on the recovery of neurological function after spinal cord injury in rats

2001 ◽  
Vol 363 (1) ◽  
pp. 94-100 ◽  
Author(s):  
Toshio Suzuki ◽  
Hozumi Tatsuoka ◽  
Tanemichi Chiba ◽  
Toshihiko Sekikawa ◽  
Tetsuharu Nemoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nitric Oxide Synthase ◽  
Neurological Function ◽  
Beneficial Effects ◽  
Cord Injury ◽  
Oxide Synthase

NAD(P)H oxidase, superoxide dismutase, catalase, glutathione peroxidase and nitric oxide synthase expression in subacute spinal cord injury

2004 ◽  
Vol 995 (1) ◽  
pp. 76-83 ◽  
Author(s):  
Nosratola D Vaziri ◽  
Yu-Shang Lee ◽  
Ching-Yi Lin ◽  
Vernon W Lin ◽  
Ram K Sindhu
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Glutathione Peroxidase ◽  
Cord Injury ◽  
Oxide Synthase

Allicin protects spinal cord neurons from glutamate-induced oxidative stress through regulating the heat shock protein 70/inducible nitric oxide synthase pathway

2015 ◽  
Vol 6 (1) ◽  
pp. 320-329 ◽  
Author(s):  
Shu-Guang Liu ◽  
Peng-Yu Ren ◽  
Guo-Yu Wang ◽  
Shu-Xin Yao ◽  
Xi-Jing He
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Heat Shock Protein 70 ◽  
Underlying Mechanism ◽  
Spinal Cord Neurons ◽  
Cord Injury ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

We demonstrate that allicin may be used as an effective treatment for spinal cord injury, and that the potential underlying mechanism involves HSP70/iNOS pathway-mediated inhibition of oxidative stress.

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