CDK5 May Be Involved In Ginsenoside Rb1 Attenuating Beta-amyloid Protein 25-35-induced Tau Protein Hyperphosphorylation In Embryo Rat Neurons

Objective To explore the effect of ginsenoside Rb1 on cyclin-dependent kinase 5 activator, p35/p25 in the process ofβ-Amyloid peptide 25-35 -induced tau hyperphosporylation.Methods Primary cultures of hippocampal neurons were prepared from the embryonic Sprague-Dawley rats, then chose an appropriate time and concentration of Aβ_25-35 ,Western blot and/or immunocytochemical staining were used to detect the levels of the cyclin-dependent kinase 5 activator-p35/p25 , cdk5 and tau phosphorylation at the sites of Thr²⁰⁵,Ser³⁹⁶ and Ser⁴⁰⁴ in hippocampal neurons.Results After exposure to Aβ_25-35 (20μmol/ L) for 12 h, the lever of p25 and p25/p35 was increased ,but the lever of protein cdk5 did not markly changed. Meanwhile, the levels of tau protein phosphorylation at the sites of Thr205,Ser396 and Ser404 were also enhanced. Pretreatment with ginsenoside Rb1 or calpeptin, a specific inhibitor of calpain, decreased the lever of p25. Pretreatment with ginsenoside Rb1 or Roscovitine, a specific inhibitor of CDK5, reduced Aβ_25-35-induced tau hyperphosphorylation.Conclusion p25/cdk5 may be involved in Ginsenoside Rb1 attenuatingβ-Amyloid peptide 25-35 -induced tau hyperphosporylation.