Dimethyl sulfoxide provides neuroprotection in a traumatic brain injury model
AM Di Giorgio, Y Hou, X Zhao, B Zhang… - Restorative …, 2008 - content.iospress.com
AM Di Giorgio, Y Hou, X Zhao, B Zhang, BG Lyeth, MJ Russell
Restorative neurology and neuroscience, 2008•content.iospress.comPurpose: 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 …
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 …
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.
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