Investigation of the neuroprotective effect of punicic acid application after acute traumatic brain injury in rats

Objective: Traumatic Brain Injury (TBI) is an important cause of death and disability worldwide, especially in children and young adults. TBI can be classified by severity, mechanism, or other characteristics. Inflammation, apoptosis, oxidative stress and ischemia are some of the important pathophysiological mechanisms underlying neuronal loss after TBI. Punicic Acid (PA) is an anticonvulsant compound approved for the adjunctive treatment of partial onset seizures and neuropathic pain. This study aimed to investigate possible neuroprotective effects for PA in a rat model of TBI. Materials and methods: Forty adult male Wistar albino rats were used. Rats were divided into 5 groups (n: 8). Group 1: Control group, Only skin incision was made. Group 2: The sham group included only normally fed rats after TBI. Group 3: After TBI, 1 g/day PA was given by gavage in addition to the normal diet. Group 4: 3 g/day PA, Group.5: 5 g/day PA was used. Brain samples were collected 3 days after TBI for each group. Brain samples and blood were evaluated by histopathological and biochemical methods. Immunohistochemistry results were confirmed by western blot. In addition, electroencephalography monitoring results were compared. Results: Malondialdehyde (MDA) levels, which are oxidative stress markers, decreased with PA treatment, while superoxide dismutase (SOD) increased. iNOS and eNOS immunoreactivity were significantly (P<0.05) reduced with PA treatment compared to TBI samples. VEGF for vascularization increased significantly (P<0.05) with PA compared to TBI group. The distribution of HIF-1α for hypoxia decreased significantly (P<0.05) with PA compared to the TBI group. NeUN for mature neuron nuclei increased significantly (P<0.05) with PA compared to TBI group. The delta power of EEG in the group treated with PA was similar to the values of the control group. Conclusion: It showed that the beneficial effect of PA application after TBI, demonstrated by histological, immunohistochemical, biochemical, western blot and EEG, may have clinical significance. It was thought that this effect would increase the patient's quality of life.