Influence of acute ethanol intoxication on neuronal apoptosis and Bcl-2 protein expression after severe traumatic brain injury in rats.
- Author:
Min HE
1
;
Wei-Guo LIU
;
Liang WEN
;
Hang-Gen DU
;
Li-Chun YIN
;
Li CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Brain Injuries; Cerebral Cortex; cytology; Disease Models, Animal; Ethanol; poisoning; Immunohistochemistry; In Situ Nick-End Labeling; Male; Neurons; physiology; Prosencephalon; cytology; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Traumatology 2013;16(3):136-139
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the influence and mechanism of acute ethanol intoxication (AEI) on rat neuronal apoptosis after severe traumatic brain injury (TBI).
METHODSNinety-six Sprague-Dawley rats were randomly divided into four groups: normal control, AEI-only, TBI-only and TBI+AEI (n equal to 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 assay and immunohistochemical method, respectively.
RESULTSApoptotic 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 less than 0.05). Compared with TBI-only group, the two indexes were much higher in TBI+AEI group at all time points (P less than 0.05).
CONCLUSIONOur findings suggest that AEI can increase neuronal apoptosis after severe TBI.
