摘要
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: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury of moderate severity. bcl 2, bcl x, and bax protein expressions were detected by immunohistochemistry. 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.
