Background
The
Conclusions
Dexmedetomidine administered during the early stage of traumatic brain injury may inhibit caspase-3 cleavageHowever, the mechanism does not seem to be related to the improvement of MDA or GSH levels.
Methods
Eighteen rats were randomized into three groups: the trauma group received anesthesia, followed by head trauma with a Mild Traumatic Brain Injury Apparatus; the Trauma+Dex group received an additional treatment of 100 µg/kg intraperitoneal dexmedetomidine daily for three days; the Control group received anesthesia only.
Results
The highest MDA levels compared to the Control group were found in the Trauma group. Mean levels in the Trauma+Dex group were lower, albeit still significantly high compared to the Control group. Glutathione levels were similar in all groups. Na/K-ATPase levels were significantly lower in the Trauma group compared to both the Control group and the Trauma+Dex group. Histopathologic findings of tissue degeneration including edema, vascular congestion and neuronal injury, and cleaved caspase-3 levels were lower in the Trauma+Dex group compared with the Trauma group. Conclusions: Dexmedetomidine administered during the early stage of traumatic brain injury may inhibit caspase-3 cleavageHowever, the mechanism does not seem to be related to the improvement of MDA or GSH levels.