OBJECTIVETo observe the phenomenon of delayed neuron death secondary to traumatic brain injury, and the protective effect of p53 antisense oligonucleotide against neuron apoptosis secondary to traumatic brain injury.

METHODSThis study was based on the rat diffuse brain trauma model established by a simple weight-drop device. The behavior scales of neural function of rats and TUNEL that examined the injury extent of DNA in the cortex were used as a general assessment of brain injury. Electron microscope was used to observe the histological and cellular morphology. mRNA and protein expression of p53 were detected by in situ hybridization and immunohistochemistry. In this model, the therapeutic effect of p53 antisense drug were observed.

RESULTSFollowing trauma, the behavior scores of rats decreased rapidly and remarkably. Apoptotic neurons appeared in the traumatized cortex as early as 2 hours after impact, and peaked at 24 hours. As early as 2 hours after impact, p53 mRNA and p53 protein in the cortex were expressed increasingly.

CONCLUSIONNeural apoptosis plays an important role in delayed neuron death and is responsible for neural dysfunction following traumatic brain injury. So the inhibition of neural apoptisis would turn into a new therapic measure against delayed neuron death following traumatic brain injury.