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Objective: Traumatic brain injury (TBI) is associated with high mortality and morbidity. Trauma-induced primary damage is followed by apoptosis, lipid peroxidation and oxidative stress that lead to secondary damage, causing exacerbation of TBI. In various inflammation models, dexpanthenol was shown to protect tissues against oxidative damage. It was aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI model. Methods: Wistar albino male rats were randomly assigned to control (n = 8), TBI+dexpanthenol (500 mg/kg; n = 10) and TBI+vehicle (n = 10) groups. TBI was performed under anesthesia (ketamine+xylazine) by dropping a 300 g weight from 70- cm height on the skull of rats, which were injected intraperitoneally with vehicle or dexpanthenol immediately after trauma. At 24th h of trauma, rats were decapitated. Malondialdehyde (MDA) -indicative of lipid peroxidation-, myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) levels and catalase (CAT) activities and levels of luminol- and lucigenimmediated chemiluminescence (CL), -indicating presence of reactive oxygen species- were measured in brain tissues. Following transcardiac parafolmadehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. The data was evaluated by one-way ANOVA. Results: In the vehicle-treated TBI group, MPO level, caspase- 3 activity and luminol-lucigenin CL levels were elevated (p<0.05-0.001), while in the dexpanthenol-treated TBI group these increases were suppressed (p<0.05-0,001) and MDA levels were decreased (p<0.05). Decreased SOD and CAT activities (p<0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol-treated TBI group (p<0.05- 0.001). Neuronal damage observed microscopically in the cortices of TBI was relatively less in the dexpanthenol-treated group. Conclusion: Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and thereby alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. [ABSTRACT FROM AUTHOR]

Objective: Oxidative stress following traumatic brain injury (TBI) leads to further deterioration of brain damage. Mildronate, known for its vasodilator and anticonvulsant effects, has been shown to be useful in a variety of experimental models and ischemic diseases. In this study, it was aimed to investigate possible antioxidant and neuroprotective effects of mildronate in a rat TBI model. Methods: Under ketamine anesthesia, TBI (n=20) was induced by dropping a metal weight (300 g) from a height of 70 cm on the skull of male Wistar albino rats. Half of the rats was treated intraperitoneally with vehicle, while the other half was treated with mildronate (100 mg/kg) immediately after TBI. Control group (n=8) was not exposed to any trauma. Twenty-four hours after TBI, transcardial paraformaldehyde perfusion was performed and brain injury was graded histopathologically following hematoxylin-eosin staining. Activities of myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) and catalase (CAT), and levels of luminol- and lucigenin-enhanced chemiluminescence (CL) were measured in brain tissues. The data were evaluated by one-way ANOVA. Results: In the mildronate-treated group, the damage in the cerebral cortex that has occurred due to TBI was lighter compared to that of the vehicle-treated TBI group. Antioxidant SOD activity, which was found to be decreased in the brain tissues of the vehicle-treated TBI group (p<0.01), was increased in the group that has received mildronate treatment (p<0.05). Higher levels of CL, increased MPO and caspase-3 activities (p<0.01- 0.001) in the vehicle-treated TBI group were found to be suppressed in the mildronate-treated group (p<0.05-0.001). Conclusion: Suppression of oxidative damage and apoptosis in brain tissues of rats in mildronate-treated TBI group, and alleviation of brain damage by stimulating antioxidant systems suggest that mildronate should be further evaluated for its possible therapeutic effect in traumatic brain injury. [ABSTRACT FROM AUTHOR]