Affiliations: Aaken Laboratories, Davis, CA, USA | Department of Neurological Surgery, University of
California, Davis, CA, USA | Department of Pharmacology, Shandong University School
of Medicine, Jinan, Shandong, P.R. China
Note: [] Corresponding author: Bruce G. Lyeth, Ph.D., Department of
Neurological Surgery, 1515 Newton Court, One Shields Avenue, University of
California Davis, Davis, CA 95616-8797, USA. Tel.: +1 530 754 5244; Fax: +1 530
754 5125; E-mail: bglyeth@ucdavis.edu
Abstract: Purpose: The objective of this study was to evaluate the
neuroprotective potential of the antioxidant, curcumin compared to α-tocopherol
in a rat model of traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were administered curcumin
(3, 30, 300 mg/kg), α-tocopherol (100 mg/kg), DMSO vehicle, or saline,
30 min prior to and 30 and 90 min after moderate lateral fluid percussion TBI.
Rats were euthanized at 24 hours after injury and coronal brain sections were
stained with Fluoro-Jade to identify degenerating neurons. Degenerating neurons
in the CA2-3 sector of the dorsal hippocampus were quantified in 10 sections
spaced 300 μm apart in each rat. Results: One way ANOVA revealed a significant difference
(p = 0.01) between groups. The curcumin, α-tocopherol, and DMSO groups
had significantly reduced numbers of degenerating neurons compared to the
saline-treated group. No significant differences were observed between any of
the drug treatment groups or the DMSO group. Conclusions: Since protection in the DMSO vehicle group was
equal to that of the experimental groups, no conclusions about neuroprotection
regarding α-tocopherol or curcumin can be made from this study. The
results suggest that DMSO may be acting as an overriding neuroprotectant in
this experiment. We conclude that DMSO is a viable neuroprotective agent
against secondary cell death in TBI.
