Cerebral protective effects of gabapentin in a rat model of head injury

Objective: Gabapentin reduces neuronal excitability, oxidative stress, release and/or synthesis of inflammatory mediators. The purpose of our study is to explore the emerging biochemical and pathological effects of gabapentin in a rat model of head injury. Materials and Methods: Thirty-two male Sprague-Dawley rats were used. The rats were randomly assigned into four distinct groups, each consisting of eight subjects: a sham group, a control group, a dexamethasone-treated group, and a gabapentin-treated group. In brain samples, assessment of malondialdehyde (MDA) levels, glutathione peroxidase (GPx), and superoxide dismutase (SOD) enzyme activities were evaluated. Results: Pathological examinations indicated that the cortical injury resulting from trauma was reduced in the group treated with gabapentin. Traumatic brain injury (TBI) led to a substantial increase in MDA levels within the tissue. Conversely, when examining the tissue SOD and GPx activities, a significant reduction was observed. The assessment of SOD and GPx activities illustrated that both the dexamethasone and gabapentin groups exhibited significantly elevated levels in contrast to the control group. Conclusion: These findings strongly suggest that gabapentin is effective in a head injury model.