Ginkgo biloba Extract 50 inhibit beta-amyloid-induced apoptosis in hippocampal neurons

Objective: To study the mechanism of Ginkgo biloba Extract 50(GBE50) inhibit beta-amyloid(Aβ)-induced apoptosis in hippocampal neurons in vitro. Methods: The primary hippocampal neuron was cultured in vitro and induced to apoptosis by 20μmol/L Aβ25-35. The MTT and flow cytometry were used to observe the effect of GBE50 with different concentrations on cell viability and apoptosis in neurons. Furthermore, the Western blot was used to detect expressions of apoptosis-related protein Bcl-2, Bax and caspase-3. Results: Compared with control group, 20μmol/L Aβ25-35 could reduce the cell vitality significantly(P0.05). There were statistical differences between GBE50 group with different concentrations(10μg/ mL except) and Aβ group(P0.05). GBE50 could improve cell vitality with certain concentration dependence. The cell apoptosis rate and necrosis rate were obviously increased by 20μmol/L Aβ25-35(P0.01). However, 50μg/mL GBE50 could significantly reduce the cell apoptosis and necrosis rate(P0.05). The result of protein detection showed that, compared with control group, 20 μmol/L Aβ25-35 could reduce the ratio of Bcl-2/Bax and enhance the activated caspase-3 expression(P0.05). But GBE50 could make this ratio of Bcl-2/Bax increase and weaken the expression of activated caspase-3 with certain concentration dependence.What's more, the statistical difference was significant between GBE50 group(50 and 100μg/mL) and the control group(P0.05). Conclusion: 20μmol/L Aβ25-35 could induce the apoptosis of hippocampal neuron. However, GBE50 could enhance the antiapoptosis protein Bcl-2 expression and reducing expressions of two pro-apoptosis proteins Bax and caspase-3, thus it could inhibit the apoptosis of neurons and improve cell vitality. These effects consequently contributed to protect hippocampal neurons.