Ginsenoside Rb1 attenuates beta-amyloid peptide(25-35) -induced hyperphosphorylation of tau protein through CDK5 signal pathway.
- Author:
Yu-Hua XIE
1
;
Xiao-Chun CHEN
;
Jing ZHANG
;
Tian-Wen HUANG
;
Jin-Qiu SONG
;
Ya-Xiu FANG
;
Xiao-Dong PAN
;
Zhi-Ying LIN
Author Information
1. Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, China.
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
antagonists & inhibitors;
Animals;
Cyclin-Dependent Kinase 5;
metabolism;
Fetus;
Ginsenosides;
isolation & purification;
pharmacology;
Hippocampus;
cytology;
Nerve Tissue Proteins;
metabolism;
Neurons;
metabolism;
Panax;
chemistry;
Phosphorylation;
drug effects;
Plants, Medicinal;
chemistry;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
tau Proteins;
metabolism
- From:
Acta Pharmaceutica Sinica
2007;42(8):828-832
- CountryChina
- Language:Chinese
-
Abstract:
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.
