Hypothermia Effect on Apoptotic Neuronal Death in Traumatic Brain Injury Model.
- Author:
Do Sung YOO
1
;
Soon Kyu LEE
;
Pil Woo HUH
;
Young Min HAN
;
Hyung Kyun RHA
;
Dal Soo KIM
Author Information
1. Department of Neurosurgery, Uijeongbu St. Mary's Hospital, The Catholic University of Korea College of Medicine, Uijeongbu, Korea. pilbrain@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Traumatic brain injury;
Apoptosis;
TUNEL assay;
Bax;
Bcl-2
- MeSH:
Animals;
Apoptosis;
bcl-2-Associated X Protein;
Body Temperature;
Brain;
Brain Injuries*;
Cell Death;
Coloring Agents;
Hippocampus;
Hypothermia*;
In Situ Nick-End Labeling;
Neurons*;
Neuroprotective Agents;
Percussion;
Rats
- From:Journal of Korean Neurosurgical Society
2005;38(3):215-220
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: Many researchers believe that the hypothermia shows neuroprotective effect on brain injury. To understand the molecular mechanism of the hypothermic treatment, this study investigated its effects on the expression of cell death or survival related proteins such as p53, Bcl-2 and Bax in the rat traumatic brain injury(TBI) model. METHODS: Twenty rats (Spraque Dawley, 200~250g) were subjected to the brain injury of moderate severity (2.4~2.6atm) using the fluid percussion injury device and five rats were received only same surgery as controls. During 30minutes after the brain injury, the hypothermia group was maintained the body temperature around 34 degrees C while the control group were maintained that of 36 degrees C. Five rats in each group were sacrificed 12h or 24h after brain injury and their brain sections was analyzed for physical damages by H-E stains and the extent of apoptosis by TUNEL assay and immunohistochemical stains. The tissue damage after TBI was mainly observed in the ipsilateral cortex and partly in the hippocampus. RESULTS: Apoptosis was observed by TUNEL assay and the Bax protein was detected in both sample which harvested 12h and 24h after TBI. In the hypothermia treatment group, tissue damage and apoptosis were reduced in HE stains and TUNEL assay. In hypothermia treatment group rat shows more expression of the Bcl-2 protein and shows less expression of the Bax protein, at both 12h and 24h after TBI. CONCLUSION: These results show that the hypothermia treatment is an effective treatment after TBI, by reducing the apoptotic process. Therefore, it could be suggested that hypothermia has a high therapeutic value for treating tissue damages after TBI.
