Riboflavin Treatment Reduces Apoptosis and Oxidative DNA Damage in a Rat Spinal Cord Injury Model

Abstract

Objective: Spinal cord injury (SCI) leads to an inflammatory response and results in oxidative stress, which has deleterious effects on several organ systems. Riboflavin is an easily absorbed micronutrient that plays an important role in maintaining health in humans and animals. The present study was designed to investigate the putative protective effect of riboflavin against SCI-induced spinal cord and kidney damage. Methods: In order to induce SCI, the standard weight-drop method was used to induce a moderately severe injury (100 g/cm force) at the T10 vertebral level. Injured animals were given either 25 mg/kg riboflavin or carboxymethyl cellulose 15 min after injury, and this regimen was repeated twice daily for 7 days. On the 7th post-injury day, a neurological examination was performed and rats were sacrificed. Spinal cord and kidney samples were harvested and prepared for a histological examination. Tissue levels of malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) and activities of myeloperoxidase (MPO), superoxide dismutase (SOD), and caspase-3 were determined. Results: SCI caused a significant decrease in tissue GSH levels and SOD activities, which were accompanied by significant increases in MDA and 8-OHdG levels and MPO and caspase-3 activities. However, riboflavin treatment reversed these parameters and improved histological findings. Conclusion: SCI caused tissue injury through oxidative stress and neutrophil infiltration into tissues. Riboflavin inhibited tissue injury through its neuroprotective and antiapoptotic effects. Moreover, our study demonstrated that riboflavin not only exerts antioxidant and antiapoptotic effects on the spinal cord but also has a significant impact on preventing kidney damage secondary to SCI.