Apoptosis of brain cells and expression changes of bcl-2 gene family after traumatic brain injury in rats

Objective:To investigate the apoptosis of brain cells and expression changes of bcl-2 gene family after traumatic brain injury(TBI)in rats,and to study the mechanism of secondary brain injury after TBI.Methods:After TBI model of rats were established,the apoptosis of brain cells and expression levels of bcl-2 and bax gene in injured brain side(cortex,hippocampus area,etc)in 1～14 days were evaluated by TdT-mediated dUTP nick end labeling(TUNEL)and immunohistochemistry(IHC),respectively.The relationship between TUNEL and IHC staining results was also analyzed.Results:TUNEL staining results showed that apoptotic cells were widespread in brain after TBI,and there were more apoptotic cells in injured cortex(IC)and hippocampus CA area(CA)than those in normal areas.The number of apoptotic cells increased on the first day after TBI,reached peak on the third day,and then declined gradually in seven to fourteen day after TBI.IHC staining results demonstrated that the expression levels of bcl-2 and bax gene increased significantly in brain after TBI.Moreover,their increasing and decreasing time points were similar to those of apoptotic cells.The expression levels of bcl-2 and bax gene were positively correlated with the number of apoptotic cells.Conclusion:Apoptosis may contribute to the brain cells death,and both the bcl-2 and bax expression appears to increase after TBI.The bcl-2 expression can inhibit the apoptosis,but the bax expression can promote the apoptosis through up-regulation of the apoptosis after TBI and it may be an important factor for cells death after brain trauma.