Abstract: Objective To explore the protein kinase/protein phosphatase imbalance induced by amyloid β（Aβ） and to observe the intervention role of Ginsenoside Rb1 in neonatal neural cells. Methods The neural stem cells(NSCs) were prepared after isolated from the newborn rat hippocampus and cultured. After 7 d induction the NSCs differentiated into neural cells were randomly divided into three groups: Aβ25~35 group was treated with 20 μmol/L Aβ25~35 for 12 h; Rb1+Aβ25~35 group was preconditioned with 10 μmol/L Rb1 for 24 h and then treated with 20 μmol/L Aβ25~35 for 12 h; control group was given nothing else. RT-PCR and immunofluorescence cytochemistry were used to detect the expression of protein kinase/protein phosphatase and tau. Results Compared with control group, in Aβ25~35 group glycogen synthase kinase 3β(GSK-3β) and cyclin dependent kinase 5(CDK-5) mRNA were higher, protein phosphatase 2A(PP2A) mRNA was lower; the expression of GSK-3β(pY279,216) was higher and PP2A was lower under fluorescence microscope; the positive cell rates of microtubule associated protein Tau(pS396) and Tau(ps262) were higher(p<0.05). Rb1 pretreatment can depress the changes of phosphotase/phosphorylase and tau mentioned above induced by Aβ25~35. Conclusions Aβ25~35 induces phosphotase/phosphorylase imbalance and tau hyperphosphorylation in neonatal neural cells which can be depressed by Rb1.

Key words: Neonatal neurons, Ginsenoside Rb1, amyloid β, Tau, phosphorylation