Abstract
One of the most pronounced phenomena of spinal cord injury (SCI) pathology is various changes caused by oxidative stress due to secondary damage. In recent years, it has been understood that valproic acid (VPA) has neuroprotective properties other than its clinical effect. The aim of this study is to investigate whether there is a change in antioxidant activity and trace the element level due to SCI-induced secondary damage, and to examine whether VPA has an effect on this change. Experimentally, spinal damage was induced in a total of sixteen rats by compressing the infrarenal and iliac bifurcation parts of the aorta for 45 minutes and these rats were equally divided into SCI (control) and SCI + VPA groups. The treatment group was injected with VPA (300 mg/kg) intraperitoneally once following SCI. In addition, the motor neurological functions of both groups after SCI were evaluated with the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and Rivlin's angle of incline test. The spinal cord tissues of both groups were homogenized and the supernatants were separated for biochemical analysis. The results showed that SCI significantly reduced catalase (CAT), glutathione peroxidase (GPx), total antioxidant status (TAS), magnesium (Mg), zinc (Zn) and selenium (Se) levels and increased total oxidative status (TOS), oxidative stress indices (OSI), chromium (Cr), iron (Fe), and copper (Cu) in damaged spinal cord tissue. In particular, the administration of VPA prior to the significant increase in the effect of SCI-secondary damage turned these negative findings into positive. Our findings show that the spinal cord tissue damaged during SCI is protected against oxidative damage thanks to the neuroprotective property of VPA. Furthermore, it is an important finding that this neuroprotective mechanism contributes to the maintenance of the level of essential elements and antioxidant activity against SCI-induced secondary damage.
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