Abstract: Objective: To explore the retinal ganglion cells (RGCs) pathological changes and expression of Bax, P53 and caspase3 protein in RGCs after the damage of the traumatic optic nerve injury in rats at different time points, to investigate the mechanism of traumatic optic nerve injury and the role of pro-apoptotic genes. Methods: the animal model of optic nerve injury in rats was built by fluid percussion brain injury device (FPI). Rats were killed on 1,3,5,7,9,14,28 days after injury. The changes of RGCs were observed by histopathology, the expression of Bax, P53 and caspase3 in RGCs were studied by immunohistochemistry method. Results: On the first day after the optic nerve injury the number of RGCs reduced. On the seventh day after the injury the number of RGCs decreased rapidly. On the fourteenth day after the injury the number of RGCs decreased slowly. On the twenty eighth day after the injury the number of RGCs stabilized. Expression of P53, Bax and Caspase3 mRNA increased in RGCs after the injury. The expression of those increased more significantly in the injury group than in control group (P<0.05). Conclusion: The decrease in the number of RGCs after the optic nerve injury is an important pathological basis in the degression of visual function. Apoptosis is one of the mechanisms of the death of RGCs. The pro-apoptotic protein P53, Bax and Caspase3 play an important role in RGCs apoptosis .

Key words: traumatic optic nerve injury, pro-apoptotic gene, P53, Bax, caspase3