JNK/p38 MAPK involves in ginsenoside Rb1 attenuating beta-amyloid peptide (25-35) -induced tau protein hyperphosphorylation in embryo rat cortical neurons.
- Author:
Jin-Qiu SONG
1
;
Xiao-Chun CHEN
;
Jing ZHANG
;
Tian-Wen HUANG
;
Yu-Qi ZENG
;
Jie SHEN
;
Li-Min CHEN
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;
Cells, Cultured;
Cerebral Cortex;
cytology;
metabolism;
Ginsenosides;
isolation & purification;
pharmacology;
JNK Mitogen-Activated Protein Kinases;
metabolism;
Neurons;
metabolism;
Panax;
chemistry;
Peptide Fragments;
antagonists & inhibitors;
Phosphorylation;
Plants, Medicinal;
chemistry;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
p38 Mitogen-Activated Protein Kinases;
metabolism;
tau Proteins;
metabolism
- From:
Acta Pharmaceutica Sinica
2008;43(1):29-34
- CountryChina
- Language:Chinese
-
Abstract:
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.
