Effects of p53 expression in hippocampus on nerve cell apoptosis after traumatic brain injury in rats

AIM: To explore the mechanism of delayed neuronal death after traumatic brain injury (TBI) and probe into the effects of Cyclophosphamide (CTP) on rats after TBI. METHODS: The model of severe closed traumatic brain injury was used and the expression of p53 protein and nerve cell apoptosis in hippocampus were dynamically observed in rats after TBI by means of immunohistochemistry and TUNEL. RESULTS: The expression of p53 protein and apoptosis positive cells were not found in the hippocampus of the fake operation group and the normal group. The expression of p53 protein was found in the area of CA2 in hippocampus at 3 h after TBI in rats, which reached the peak at 24 h (A=0.149±0.016) and decreased at 72 h. Some apoptosis positive cells appeared in the area of CA2 in hippocampus in rats at 24 h after TBI, which reached the peak at 168 h (29.2±4.7/HP) and decreased at 336 h. The peak of the p53 protein ( A =0.106±0.017)expression and apoptosis(21.0±4.6/HP) in CTP group were obviously lower than those in TBI group. CONCLUSION: The increased expression of p53 protein may bring about nerve cell apoptosis after TBI. CTP can reduce the expression of p53 protein and restrain nerve cell apoptosis.