Objective: To study the effects of Ginkgo biloba extract ( GBE) on lipid peroxidation and apoptosis after spinal cord ischemia/reperfusion (I/R) in rabbits. Methods: Spinal cord I/R injury model was established according to the description of Erten et al. A total of 27 New Zealand white rabbits were divided into three groups randomly: a sham group (9 rabbits treated with sham operation but without aortic occlusion) . a model group (9 rabbits treated with aortic occlusion and volume-matched saline) , and a GBE group (9 rabbits treated with aortic occlusion and Ginaton (100 mg/ kg) injected 30 minutes before aortic clamping and at the onset of reperfusion). The neurological outcomes were evaluated at 24 and 48 hours after reperfusion, respectively. The spinal cord malondialdehyde ( MDA) level, superoxide dismutase ( SOD) were then detected. Neural cell apoptosis was determined by terminal deoxynucleotidyl transferase ( TdT ) -mediated dUTP-fluorescence nick end labeling ( TUNEL) method and the expression of bcl-2 and bax were examined histologically in the spinal cord with immunohistochemistry. Results: I/R produced a significant decrease in neurological scoring. The motor scores of the GBE group were significantly higher than those of the model group at 24 and 48 hours after reperfusion (P<0.05). Compared with the model group, GBE ameliorated the down-regulation of SOD and produced a significant reduction of the MDA level ( P <0.01). The positive cells for TUNEL in the model group were much more than those of the GBE group (P<0.01). The bcl-2 was up-regulated after I/R, especially in the GBE group (P<0.01). The up-regulation of bax was greatly diminished by GBE (P<0.01). Conclusions: GBE has protective effects against spinal cord I/R injury, and the mechanism may be that it can scavenge oxygen free radicals and inhibit the apoptosis of neural cells. Objective: To study the effects of Ginkgo biloba extract (GBE) on lipid peroxidation and apoptosis during myopic cord ischemia/reperfusion (I/R) in rabbits. Methods: Spinal cord I/R injury model was established according to the description of Erten et a. A total of 27 New Zealand white rabbits were divided into three groups randomly: a sham group (9 rabbits treated with sham operation but without aortic occlusion) . a model group (9 rabbits treated with aortic occlusion and volume-matched saline), And a GBE group (9 rabbits treated with aortic occlusion and Ginaton (100 mg/ kg) injected 30 minutes before aortic clamping and at the onset of reperfusion). The neurological outcomes were evaluated at 24 and 48 hours after reperfusion, respectively. Cord malondialdehyde (MDA) level, superoxide dismutase (SOD) were then detected. Neural cell apoptosis was determined by terminal deoxynucleotidyl transferase ( TdT ) -mediated dUTP-fluorescence nick end labeling ( TUNEL) method a Results of I/R produced a significant decrease in neurological scoring. The motor scores of the GBE group were significantly higher than those of the model group at 24 nd the expression of bcl-2 and bax were examined histologically in the spinal cord with immunohistochemistry. And 48 hours after reperfusion (P<0.05). Compared with the model group, GBE ameliorated the down-regulation of SOD and produced a significant reduction of the MDA level ( P <0.01). The positive cells for TUNEL in the model group were Much more than those of the GBE group (P<0.01). The bcl-2 was up-regulated after I/R, especially in the GBE group (P<0.01). The up-regulation of baxster was significantly reduced by GBE ( P<0.01). Conclusions: GBE has protective effects against spinal cord I/R injury, and the mechanism may be that it can scavenge oxygen free radicals and inhibit the apoptosis of neural cells.