Studies indicated that oxidative stress induced by cerebral hemorrhage might affect the neuronal cell apoptosis and c-myc protein overexpression. 100 rats were random equally to two groups-test and control. Each group was set 5 time points at 6 h, 12 h, 24 h, 48 h and 72 h after administration, respectively. After hydraulic brain injury rat model was successfully established, animals in test group were given a single intravenous injection with 5 mg/L/kg mono-methoxy polyethylene glycol modified-SOD (MPEG-SOD), while animals in control group were injected with isotonic saline. The rate of neuronal cell apoptosis, the expression level of c-myc protein, and the correlationship between them were analysed. Cell edema and widened gap occurred in brain at 6 h, and the most obvious brain damage appeared at 48 h after cerebral hemorrhage in test group. The number of TUNEL-positive cells in test group at each time point were significantly less than those in control group (P<0.01). The gray values of c-myc protein in test group at each time point were lower than those in control group (P<0.01). The number of TUNEL-positive nerve cells and the gray level of c-myc protein were correlated ( test group R-2 = 0.857, control group R-2 = 0.654, P<0.01). The cell apoptosis rates in test group were significantly lower than those in control group (P<0.01). In onclusion, while oxidative stress plays a key role in neuronal death after traumatic brain injury, MPEG-SOD inhibits the increase the overexpression of c-myc protein, and prevents neuronal cell apoptosis.