Objective The exact pathogenesis of cerebral ischemia-reperfusion injury (CIRI) remains unclear. This study explored whether ginkgo biloba extract (GBE) can improve neurological function in a CIRI rat model and the related mechanisms. Methods The CIRI rat model was induced by middle cerebral artery occlusion for 2 h, followed by reperfusion for 22 h. Varying dosages of GBE were administered intraperitoneally for 15 days. Subsequently, CIRI model rats were scored for neurological function to evaluate the effect of GBE on their motor function. In addition, 2,3, 5-triphenyltetrazolium chloride staining was used to detect the volume of infarcted brain, Western blot was used to detect expression of autophagy marker proteins and apoptosis-related proteins, the serum activities of superoxide dismutase (SOD) and glutathione (GSHpx) and serum level of malonaldehyde was detected by ELISA. Results GBE significantly improved the neurological function scores of CIRI model rats, markedly reduced cerebral infarction volumes, and significantly upregulated the activities of serum SOD and GSH-px, while decreasing the level of MDA. In addition, GBE significantly increased protein expression of Beclin-1 and protein expression ratios of LC3-II/ LC3-I and Bcl-2/ Bax, while remarkedly reducing protein expression of Caspase-3. Conclusions GBE improved the motor dysfunction of CIRI model rats by inhibiting oxidative stress and apoptosis, as well as activating the autophagy system to achieve a protective effect on brain cells.