JNK/p38 MAPK involves in ginsenoside Rb1 attenuating beta-amyloid peptide (25-35)-induced tau protein hyperphosphorylation in embryo rat cortical neurons

To explore the effect of ginsenoside Rb1 on JNK/p38 MAPK in the process of β-amyloid peptide (25-35) -induced tau protein hyperphosphorylation, Western blotting and immunocytochemical stain were performed to observe the tau protein phosphorylation and the expression of JNK/p38 MAPK. The level of tau protein phosphorylation in the sites of Ser³⁹⁶, Ser^199/202 and Thr²⁰⁵ increased after rat cortical neurons exposed to 20 μmol·L^-1 Aβ_25-35, meanwhile the level of JNK/p38 MAPK also increased after Aβ_25-35 treatment for 12 h. Pretreatment with several doses of ginsenoside Rb1 markedly attenuated tau protein hyperphosphorylation and the expression of JNK/p38 MAPK. Ginsenoside Rb1 markedly attenuated tau protein hyperphosphorylation through JNK/p38 MAPK pathway.