Citation

Bailey ZS, Nilson E, Bates J, Oyalowo A, Hockey KS, Sajja S, Thorpe C, Rogers H, Dunn B, Frey AS, Billings MJ, Sholar CA, Hermundstad A, Kumar C, Vandevord PJ, Rzigalinski BA. J. Neurotrauma 2016; ePub(ePub): ePub.

Affiliation

Edward Via Virginia College of Osteopathic Medicine, NanoNeuroLab , Res. II Bldg - Corp. Res. Ctr , 1861 Pratt Drive , Blacksburg, Virginia, United States , 24060 ; brzigali@vcom.vt.edu.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2016.4644

PMID

27733104

Abstract

Mild traumatic brain injury results in aberrant free radical generation, which is associated with oxidative stress, secondary injury signaling cascades, mitochondrial dysfunction, and poor functional outcome. Pharmacological targeting of free radicals with antioxidants has been examined as an approach for treatment, but has met with limited success. Conventional antioxidants currently available scavenge a single free radical, before they are destroyed in the process. Here, we report for the first time, that a novel regenerative cerium oxide nanoparticle antioxidant reduces neuronal death and calcium dysregulation after in vitro trauma. Further, using an in vivo model of mild fluid percussion brain injury in the rat, we report that cerium oxide nanoparticles also preserve endogenous antioxidant systems, decrease macromolecular free radical damage, and improve cognitive function. Taken together, our results demonstrate that cerium oxide nanoparticles are a novel nanopharmaceutical with potential for mitigating neuropathological effects of mild traumatic brain injury and modifying the course of recovery.

Language: en