Evaluation of minocycline's neuroprotective effects in experimental spinal cord injury

Traumatic spinal cord injury (SCI) is a devastating problem of health that results in high morbidity and mortality rates. The loss of function after SCI results from both the primary mechanical insult and the subsequent, multifaceted secondary response. We therefore evaluated the neuroprotective effects of minocycline on the secondary injury process of an experimental traumatic spinal cord injury model. All experiments were conducted in the animal laboratory of Baskent University by the approval of Baskent University Animal Care Ethics Committee. A total of 80 adult male Spraque Dawley rats were randomly divided to four groups. A thoracal 9-10 contusion injury was produced by using modified Allen technique in all groups except control group. No medication was administered to the rats in the trauma group. Minocycline was administered intraperitoneally and intravenously to the treatment groups. Short term and long term neuroprotective effects of minocycline on the lipid peroxidation (MDA, GSH), apoptosis (TUNEL), ultrastructure of spinal cord (EM, LM) and behavioral assesments (BBB, Inclined plane) were evaluated.Our study demonstrated that minocycline significantly diminishes lipid peroxidation, reduce apoptosis and preserves the ultrastructure of spinal cord tissue in the early posttraumatic period. Behavioral assesments showed significant improvement on the hind limb functions of minocycline receiving rats. Any statistically significant difference was not found between intaperitoneal or intravenous routes for minocycline injection. We report that minocycline is neuroprotective and contributes to functional improvement after traumatic SCI by eliminating the destructive process of secondary injury. The encouraging results of minocycline in experimental models bode well for its therapeutic use in the injuries of human spinal cord.