Introduction: Traumatic spinal cord injury (TSCI) is a condition caused by irreversible damage on neurological function. One mechanism observed after TSCI is apoptosis, inducing the loss event of adjacent healthy tissue. Therefore, the search for treatments aimed at reducing the process is paramount. Dapsone (DDS) is a drug capable of inhibiting oxidative damage, inflammatory response after a process of ischemia/reperfusion in rats. Previously in the laboratory showed that the DDS protects tissue damage and promotes functional recovery in rats.
Objective: To evaluate the antioxidant effect of dapsone based on the reduced amount present in the acute phase after trauma in a rat model glutathione.
Method: Female Wistar rats (200-250g) were used, being assigned randomly into 11 groups: sham 4 groups (n=16), 7 groups of rats with TSCI (n=56). The animals were anesthetized with pentobarbital and underwent a laminectomy or TSCI level T-9 using the New York University team Spinal Cord Impactory. Subsequently, three different doses of Dapsone depending the group they belonged to (12.5, 25 and 37.5 mg/kg) were administered. The animals were sacrificed 24 hours after surgery.
Results: The values obtained from the analysis of the amount of GSH in the injured groups are similar no significant when compared with the control group (TSCI+Vehicle) differences.
Conclusions: The findings of this study showed that the antioxidant effect of dapsone is unrelated to the regulation of GSH, because there is no reduction in the neurodegenerative effects when using dapsone treatment in the acute phase of TSCI (first 3-5 hours), so that the evaluation of other markers of oxidative damage is suggested.