Objective To study the effect of Ginkgo biloba Extract 50 (GBE50) on beta-amyloid(Aβ)-induced apoptosis and oxidative stress in hippocampal neurons in vitro. Methods The primary hippocampal neuron was cultured in vitro and reduced to apoptosis and oxidative stress by 20 μM Aβ25-35. The MTT, flow cytometry and fluorescent probes labeling were used to observe the effect of GBE50 with different concentrations on cell viability, apoptosis and generation of intracellular reactive oxygen species (ROS) in neurons. Results (1) 20 μM Aβ25-35 could reduce the cell vitality significantly (P < 0.05). There was statistical difference between GBE50 group with different concentrations (10 μg/ml except) and Aβ group (P < 0.05). GBE50 could improve cell vitality with certain concentration dependence. (2) The cell apoptosis rate and necrosis rate were obviously increased by 20 μM Aβ25-35 (P < 0.01) and higher about 14.5% and 8.6% respectively. However, 50 μg/ml GBE50 could significantly reduce the cell apoptosis and necrosis rate (P < 0.05) and lower about 47.7% and 59.5% respectively. (3) The result of intracellular reactive oxygen species generation detected by fluorescent probes DCFH-DA show that the statistical difference was observed between Aβ group and control group (P < 0.05) , and 20 μM Aβ25-35 could enhance ROS. However, any difference wasn’t detected between every concentration of GBE50 group and control group(P > 0.05). Conclusions The 20 μM Aβ25-35 could induce hippocampal neuron apoptosis and generations of intracellular ROS, which were inhibited by GBE50 with different degrees. Through these effects and improving cell vitality, GBE50 could availably protect hippocampal neurons. KEYWORDS Ginkgo biloba extract 50; beta-amyloid; hippocampal neuron; apoptosis; oxidative stress