HE Min,LIU Wei-guo,WEN Liang,DU Hang-gen,YIN Li-chun,CHEN Li.[J].Chin J Traumatol,2013,16(1):136-139. [doi]
Influence of acute ethanol intoxication on neuronal apoptosis and Bcl-2 protein expression after severe traumatic brain injury in rats
  
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KeyWord: Craniocerebral trauma  Apoptosis  Alcoholism
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Author NameAffiliation
HE Min Department of Neurosurgery, Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310005, China 
LIU Wei-guo Department of Neurosurgery, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China 
WEN Liang Department of Neurosurgery, First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310003, China 
DU Hang-gen Department of Neurosurgery, Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310005, China 
YIN Li-chun Department of Neurosurgery, Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310005, China 
CHEN Li Department of Neurosurgery, Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310005, China 
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Abstract:
      Objective: To study the influence and mechanism of acute ethanol intoxication (AEI) on rat neuronal apoptosis after severe traumatic brain injury (TBI). Methods: Ninety-six Sprague-Dawley rats were randomly 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 suffered 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 determined by TUNEL assayand immunohistochemical method, respectively. Results: Apoptotic cells mainly distributed in the cortex 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 increase neuronal apoptosis after severe TBI.
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