Objective: To investigate the protective effects and mechanism of
ginkgolide B(银杏内酯B, GB) on neuron injury induced by cerebral
ischemia/reperfusion(I/R) in rats. Methods: The bilateral
cerebral hemisphere I/R model was established by ligating three arteries with Kameyama's manner. Fortyfive Wistar rats were randomly assigned to sham operation control, I/R model, normal saline control (NS) and GB pretreatment group. The activity of superoxide dismutase(SOD), glutathione peroxidase(GSHPx), ATPase , and the contents of malondialdehyde(MDA) in brain tissue were measured. Apoptosis of neurons and pathologic changes were observed. Results: Compared with sham operation control group,the values of SOD, GSHPx and ATPase were reduced, while MDA level increased significantly in I/R group whose neuron apoptosis index was (40 2±6 3)%. The inflammatory changes were found in brain tissue and rant order of cells wasn't clear. Previous administration of GB (110 mg/kg) could reduce MDA level and increase SOD, GSHPx and ATPase activities dosedependently( P <0 05 or P <0 01), could remarkably alleviate the brain tissue injury induced by I/R, and reduce the apoptosis index to (24 3±5 1)%, (21 0±4 2)% and (9 4±3 3)% respectively with different dosage of GB( P <0 05 or P <0 01). Conclusion: GB possesses a markedly protective effects on I/Rinduced cerebral neuron injury by reducing the production of free radicals , enhancing the free radical scavenger system and ATPase activity.