The Effects of Dendro[60]Fullerene on Neurobehavioral Outcome and Cerebral Vascular Function After Traumatic Brain Injury


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Traumatic brain injury (TBI) causes an increase in reactive oxygen species (ROS) that leads to cerebral vascular dysfunction. The reduction of ROS can preserve vascular function and lead to improved outcomes. The antioxidant carboxyfullerene nanoparticle, dendro[60]fullerene (DF-1) was examined as a potential therapy for TBI because of its strong antioxidant capabilities. The effects of DF-1 on mean arterial pressure (MAP), cerebral perfusion and cerebral vascular resistance were evaluated. DF-1’s ability to reduce neuronal cell injury after TBI was evaluated by Fluoro-Jade C staining in the hippocampus. Through these experiments a dose response curve was conducted to compare 10, 25 and 50-mg/kg doses of DF-1. 10-mg/kg was chosen as the most effective dose to be used in the remainder of experiments. Middle cerebral artery (MCA) experiments were performed to evaluate if DF-1 preserved vasodilatory responses after injury. DF-1’s effect on cerebral perfusion was also tested in a TBI + hemorrhagic hypotension model. Additionally, behavioral experiments were performed to determine if DF-1 improved cognitive performance. These experiments determined that DF-1 did not preserve vascular function, but it did result in improved performance in behavioral tests, as well as a preservation of neurons in the hippocampus after TBI. Due to the positive results in behavioral and neuropathological experiments, we believe that DF-1 deserves further examination as a therapeutic option for TBI.



Neuroscience, Nanotechnology, Antioxidants