Abstract

Objectives:To investigate the effects of syringaldehyde (SA) on the antioxidant and oxidant system in spinal cord ischemia (SCI).Methods:These study and experiments were conducted at Medical Research Center, Çanakkale Onsekiz Mart University, Çanakkale, Turkey, between 2014-2018. Eighteen New Zealand White adult male rabbits were randomly divided into 3 groups (n=6). Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), myeloperoxidase (MPO) activities, and malondialdehyde (MDA) levels were measured in the spinal cord tissues. Degenerated neurons, hemorrhage and inflammatory cell migration in the spinal cord were investigated histopathologically. Expressions of neuronal nitric oxide synthase (nNOS), caspase-3, and nuclear factor-κB (NF-κB) were evaluated immunohistochemically. Clinically, it was evaluated with Modified Tarlov score.Results:Biochemically, there was an expected decrease in SOD, CAT, and GPx enzyme activities in ischemia groups, there was also an increase in MPO activity at the same time. When the enzyme activities spinal cord ischemia/reperfusion (SCI/R)+SA, control and SCI/R groups were compared, the difference was found to be statistically significant (p<0.05). Glutathione peroxidase enzyme activity levels were very low in ischemia group compared to the significant increase in the SA group (p<0.05). Histopathologically, when SCI/R and SCI/R+SA groups were compared, there were statistically significant differences in the number of degenerative neurons and amount of hemorrhage; this comparison shows the significance of treatment in terms of inflammatory cell migration (p<0.05). The expressions of nNOS, caspase-3, and NF-κB were found significantly increased in SCI/R group compared to the control group (p<0.05). Syringaldehyde treatment decreased nNOS, caspase-3, and NF-κB expressions immunohistochemically. Clinical evaluation showed improvement in the SA-treated group.Conclusion:Syringaldehyde therapy administered for protective purposes may reduce oxidative stress, degenerative changes and inflammatory cell migration in the ischemic spinal cord.

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