Protective Effect of bcl-2Protein on Neurons following Experimental Traumatic Brain Injury in Rats

Objective To investigate the change in bcl-2,a gene inhibiting apoptosis and its role in neuronal apoptosis following traumatic brain injury(TBI).Method Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPI)of moderate severity.Bcl-2protein expression in brain tissue was detected by immunohistochemistry before the FPI and6,12,24,72,148hours after FPI.The neuronal apoptosis in the brain were detected by TUNEL and election microscope.Results Bcl-2expression was observed in the cerebral cortex,subcortical white matter,dentate gyrus,and hippocampal CA1and CA3ipsilateral to injured hemisphere.Bcl-2positive neurons displayed normal nuclei morphology;The morphological features of apoptosis or necrosis in few Bcl-2positive neurons were observed.The immunoreactivity of Bcl-2protein decreased significantly in the hippocampus ipsilateral to the impacted site as early as6h after the TBI as compared with that before the TBI.The decrease in bcl-2protein expression became relatively slow from1to3hours after TBI.Conclusion Bcl-2may play an important role in inhibiting apoptosis after TBI and may be an inducible factor protecting the neurons in the CNS.