Anti-inflammatory and anti-oxidant effect of esculetin on traumatic brain injury in rats

INTRODUCTION : Traumatic brain injury and subsequent traumatic brain damage are significant problems worldwide and in our country, leading to death and disability. Treatment options for traumatic secondary brain damage after head trauma are limited. In this study, we aimed to investigate the neuroprotective effect of esculetin, a coumarin derivative, after head trauma and its effect on oxidative stress and excessive inflammatory response leading to secondary traumatic brain damage. MATERIALS AND METHODS: An experiment was conducted by inducing head trauma in 48 male Wistar albino rats to demonstrate the effect of esculetin on traumatic secondary brain damage. The 48 rats were divided into 8 groups. Immunohistochemical staining was performed on brain tissue samples obtained from the right hemisphere after sacrifice, and histopathological changes were examined. The left hemisphere brain tissues of the rats were homogenized for ELISA analysis of Nrf-2, HO-1, and Tnf-alpha values. RESULTS: Histopathological examination revealed that neuronal degeneration was less in rats with induced head trauma and treated with esculetin, particularly in the group administered 100mg/kg (p 0.01). In the group with head trauma induction but no esculetin treatment, neuronal degeneration was more pronounced, and the number of healthy neurons was lower compared to other groups (p 0.01). No significant difference was observed between groups not subjected to head trauma and those given esculetin (p 0.05). When the ELISA results of the groups evaluating Nrf-2, HO-1, and Tnf-alpha were compared, no statistically significant difference was observed. CONCLUSION: Our study found a neuroprotective effect of esculetin in rats with induced head trauma, and this neuroprotective effect was dose-dependent on the administered esculetin. We discovered that the neuroprotective effect of esculetin in traumatic secondary brain damage was not mediated through the oxidative stress markers we used and their associated protective mechanisms.