Investigation of neuroprotective efficacy of dexpanthenol in an experimental head injury model

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model Aim: Inflammation, apoptosis and oxidative stress that develop after traumatic brain injury lead to further aggravation of damage to brain tissue. Dexpanthenol, whose neuroprotective effects are known, has been shown to be useful in various experimental models and ischemic diseases. In this study, the traumatic it is aimed to investigate the possible anti-inflammatory, antiapoptotic, antioxidant and neuroprotective effects of dexpanthenol (DXP)in a brain injury model. Material and Method: In this study, 36 Wistar-Albino female rats weighing approximately 6 months old and weighing 220-285 gr. were used. All rats were injured by reducing the weight of 350 g at an angle of 180 degrees from a height of 50 cm to the parietal region in the prepared head injury model mechanism. Rats were examined in 4 groups, 8 in the control group (Group 1), 10 in the trauma group (Group 2), 10 in the trauma+ DXP group (Group 3) and 8 in the DXP group (Group 4). In group 1, no head injury was created, DXP was not given, in group 2, a head injury was created, but DXP was not given. 30 After a head injury in Group 3.minutes, 6. it's 12 o'clock. hour, 24 hours, 36. hours and 48. DXP was administered intraperitoneally(ip) at a dose of 500 mg/kg a total of 6 times per hour. 4.the study was performed by administering DXP intraperitoneal (ip) simultaneously with group 3 without causing head trauma to the group. after 72 hours, blood samples were taken from all rats for biochemical examination, and then all rats were decapitated under general anesthesia and cerebral tissue samples were taken for immunohistochemical and histopathological examination. Results: All cytokines were increased in the post-traumatic brain tissue. Compared to the trauma group, the post-traumatic dexpanthenol group had lower malondialdehyde and glutathione reductase levels; The levels of superoxide dismutase, glutathione peroxidase and catalase were found to be significantly higher. (p<0.05) Histologically, a significant decrease was observed in the piamater layer of the brain tissue, such as congestion, cell infiltration, vascular congestion, hemorrhage and neuron degeneration in the posttraumatic dexpanthenol group compared to the trauma group. Conclusion: , We found that after head trauma in rats, DXP were beneficial in neurologic recovery on histologically and with respect to oxidative changes.The brain tissues of rats in the DXP group was suppressioned of oxidative damage and apoptosis. We suggest that DXP should be further evaluated for its possible therapeutic effect in traumatic brain injury.