ABSTRACT
OBJECTIVE: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. METHODS: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. RESULTS: The immunoreactivity of bcl-2 and bcl-x proteins decreased in the hippocampus ipsilateral impact site at 6 hours after injury, and this was the main cause of down-regulation of the value of (bcl-2+bcl-x)/ bax. During the period of 1-3 days after injury, bax protein expression increased significantly, while bcl-2 and bcl-x protein expressions decreased relatively slowly. The decreased value of (bcl-2+bcl-x)/ bax was mainly due to the bax up-regulation. CONCLUSIONS: The bcl-2 gene family is involved in neuronal apoptosis after traumatic brain injury, and the protein-expression alterations of the bcl-2 gene family members lead to apoptosis of the neuronal cells.