[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 beta-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 , Ser199/202 and Thr205 increased after rat cortical neurons exposed to 20 micromol x L(-1) Abeta25-35, meanwhile the level of JNK/p38 MAPK also increased after Abeta25-35 treatment for 12 h. Pretreatment with several doses of ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation and the expression of JNK/p38 MAPK. Ginsenoside Rbl markedly attenuated tau protein hyperphosphorylation through JNK/p38 MAPK pathway.

[Ginsenoside Rb1 attenuates beta-amyloid peptide(25-35) -induced hyperphosphorylation of tau protein through CDK5 signal pathway].

This study is to explore the effect of ginsenoside Rb1 on the process of beta-amyloid peptide(25-35) (Abeta(25-35)) -induced hyperphosphorylation of tau protein, and on the level of cyclin-dependent kinase 5 activator, p25/p35. Western blotting and/or immunocytochemical staining were used to detect the levels of phosphorylation of tau protein at the sites of Thr205, Ser396, Ser404 in hippocampal neurons, cdk5 and p25/p35. After exposure to Abeta(25-35) (20 micromol x L(-1)) for 12 h, the levels of tau protein phosphorylation at the sites of Thr205, Ser396, Ser404 were enhanced, the level of p25 was increased, but the level of protein cdk5 was not changed markedly. Pretreatment with ginsenoside Rb1 reduced Abeta(25-35) -induced hyperphosphorylation of tau protein and decreased the lever of p25, but had no effect on cdk5. Ginsenoside Rb1 can attenuate Abeta(25-35) -induced hyperphosphorylation of tau protein through CDK5 signal pathway.