Objective    To study the changes of three radicals and expression of SOD-1 in neuronal degeneration due to cerebral ischemia/reperfusion(I/R) in mice.     Methods    One hundred and sixty NIH mice were divided into I/R group and sham operation group

80 mice in each group. A cerebral I/R model was established by drawing out and reperfusing 40% of the whole blood volume and clamping the bilateral carotid arteries for 20 min. On days 5

15

30

and 60 after cerebral I/R

neuronal injury was observed under a light microscope

learning and memory ability of the mice was assessed with Morris water maze

hippocampal SOD-1 activity and malonaldehyde (MDA) level were measured with a spectrophotometer and expressions of SOD-1 mRNA and protein in the hippocampus were detected by RT-PCR and Western blotting

respectively.     Results    The MDA level

SOD-1 activity

expression level of SOD-1 protein and mRNA in sham operation group were 0.549±0.049 nmol/mg

55.134±4.076 U/mg

30.413±2.962 and 104.541±18.825

respectively. The learning and memory ability of mice was significantly lower in I/R group than in sham operation group. The MDA level in brain tissue of I/R group was significantly higher on days 5

15

30

and 60 days after I/R (0.673±0.087

0.782±0.101

0.719±0.094

and 1.084±0.140 nmol/mg) than sham operation group (P0.05). The activity of SOD-1 (42.522±3.701 and 37.011±4.843 U/mg) and the expression level of SOD-1 protein (23.145±3.476 and 15.746±2.344) were significantly lower than sham operation group after I/R on days 5 and 15 (P0.05). No significant difference was observed in SOD-1 activity after I/R 30 and 60 d between the two groups (51.801±6.706 vs 50.202±6.488 U/mg

P0.05)，while the expression of SOD-1 protein was significantly higher in I/R group than in sham operation group (44.263±6.597 vs 40.587±6.154

P0.05). However

no significant difference was found in expression level of SOD-1 mRNA (P0.05). Histology showed the progressive loss and karyopyknosis of neurons in hippocampi of I/R group.     Conclusion    Neuronal degeneration due to cerebral I/R is related with the progressively increased oxidative stress and abnormal SOD-1 expression and activity.