Study On Expression Of Bcl-2, Bax In Brain Tissue And The Level Of Serum NO, SOD In Rats After Traumatic Brain Injury

Apoptosis is a common phenomenon after traumatic brain injury (TBI), but the mechanism of apoptosis after TBI still remain enigmatic. We designed an animal experiment in an effort to determine if there were correlation between apoptosis cells, bcl-2, bax gene expression and the change of nitric oxide(NO), superoxide dismutase (SOD) after TBI.Objective: To investigate the temporal and spatial characteristics of apoptotic cells and the effects of NO, SOD on apoptotic cells death and Bcl-2, Bax expression after TBI.Method: Forty eight Wistar rats were randomly divided into eight groups, the experimental TBI model was established by Feeney's method. The brain and serum sample were taken at 2, 6, 12, 24 and 48 hours, 7,14days after TBI. Apoptosis cells were detected by terminal deoxynucleotidyl transferease-mediated biotinylated deoxyuridine triphosphate nick and labeling(TUNEL);Bcl-2/ Bax expression were inspected by immunochemical method;the quantity of nitrite and nitrate, nitric oxide end products, and enzymatic activity of SOD in serum were determined. All values were expressed as means+SD. One-way analysis of variance was used to assess group means, Pearson method to correlation analysis. P < 0.05 was considered statistically significant. Statistics were using SPSS 10.0.Result: 1.Microscope examination showed that intensive distribution of apoptosis cells could be seen in the brain tissue circulated the injured cortex, diffusive distribution in hippocampus, dentate gyrus and few apoptotic cells in brain tissue contralateral to the injured cortex and control group. Apoptotic cells were determined at 2h post injury, reached a peak at 12h, remained a high level at 24 to 48h and begandecrease slowly, still observed at 14d;2.Bcl-2 and Bax gene expression also increased after TBI. Bcl-2 protein were determined at 2h, reached its peak at 12h, then decreased slowly. The tendency of Bax similar to Bcl-2, reached its peak at 24h. 3. NO increased at 2h post injury, arrived at highest point at 12h, then decreased quickly;SOD decreased after TBI, reached lowest point at 48h. Conclusion:1. Apoptosis occurred in brain tissue after TBI. Apoptosis cells mainly distributed in the brain tissue circulated the injured cortex and also could be found in hippocampus, dentate gyrus which sensitive to ischemia and hypoxia.2. Bcl-2 and Bax expression increased following TBI. Their expression coincided with apoptosis. Increased expression of Bcl-2 and Bax contribute to apoptotic cells after TBI.3. NO increased and SOD decreased post injury indicated that there is a plenty of free radicals produced after TBI but a decline in clear ability of brain tissue. Oxidative stress plays an important role in brain damage after brain injury.4. The change of NO coincided with apoptosis cells and Bax expression following TBI. NO could enhance apoptosis cells through its effects on Bcl-2, Bax expression. Contrast to NO, SOD inhibit apoptosis.