Influence of acute ethanol intoxication on neuronal apoptosis and Bcl-2 protein expression after severe trau- matic brain injury in rats

Objective： To study the influence and mechanism of acute ethanol intoxication （AEI） on rat neu- ronal apoptosis after severe traumatic brain injury （TBI）. Methods： Ninety-six Sprague-Dawley rats were ran- domly divided into four groups： normal control, AEI-only, TBI-only and TBI＋AEI （n=24 for each）....

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Published in:中华创伤杂志：英文版 2013 (3), p.136-139
Main Author: HE Min LIU Wei-guo WEN Liang DU Hang-gen YIN Li-chun CHEN Li
Format: Article
Language:English
Subjects:
Alcoholism
Apoptosis
Craniocerebral
trauma
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Summary:Objective： To study the influence and mechanism of acute ethanol intoxication （AEI） on rat neu- ronal apoptosis after severe traumatic brain injury （TBI）. Methods： Ninety-six Sprague-Dawley rats were ran- domly divided into four groups： normal control, AEI-only, TBI-only and TBI＋AEI （n=24 for each）. Severe TBI model was developed according to Feeney＇s method. Rats in TBI＋AEI group were firstly subjected to AEI, and then suf- fered head trauma. In each group, animals were sacrificed at 6 h, 24 h, 72 h, and 168 h after TBI. The level of neuronal apoptosis and the expression of Bcl-2 protein were deter- mined by TUNEL assay and immunohistochemical method, respectively. Results： Apoptotic cells mainly distributed in the cor- tex and white matter around the damaged area. Neuronal apoptosis significantly increased at 6 h after trauma and peaked at 72 h. Both the level of neuronal apoptosis and expression of Bcl-2 protein in TBI-only group and TBI＋AEI group were higher than those in control group （P〈0.05）. Compared with TBI-only group, the two indexes were much higher in TBI＋AEI group at all time points （P〈0.05）. Conclusion： Our findings suggest that AEI can in- crease neuronal apoptosis after severe TBI.
ISSN:1008-1275