Ginsenoside Rbl attenuates beta-amyloid peptide25-35 -induced tau hyperphosphorylation in cortical neurons.
- Author:
Yu-qi ZENG
1
;
Xiao-chun CHEN
;
Yuan-gui ZHU
;
Yong-kun LI
;
Xiao-song PENG
;
Li-min CHEN
;
Jie SHEN
;
Tian-wen HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; antagonists & inhibitors; Animals; Cerebral Cortex; cytology; metabolism; Female; Fetus; Ginsenosides; isolation & purification; pharmacology; Glycogen Synthase Kinase 3; metabolism; Glycogen Synthase Kinase 3 beta; Neurons; metabolism; Panax; chemistry; Peptide Fragments; antagonists & inhibitors; Phosphorylation; Plants, Medicinal; chemistry; Rats; Rats, Sprague-Dawley; tau Proteins; metabolism
- From: Acta Pharmaceutica Sinica 2005;40(3):225-230
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo explore the effect and the possible mechanism of ginsenoside Rb1 on beta-amyloid peptide (beta-AP)(25-35) -induced tau protein hyperphosphorylation in cortical neurons.
METHODSWestern blotting and immunocytochemical staining were used to detect tau phosphorylation level, total tau and glycogen synthase kinase-3beta (GSK-3beta) in cortical neurons.
RESULTSAfter exposure to beta-AP(25-35) (20 micromol x L(-1)) for 12 h, the levels of tau protein phosphorylation in the sites of Ser 396, Ser 199/202, Thr 231 and total tau were raised. Meanwhile, the expression of GSK-3beta also increased. Pretreatment with ginsenoside Rbl or lithium chloride, a specific inhibitor of GSK-3beta, markedly reduced beta-AP(25-35)-induced tau hyperphosphorylation and the expression of GSK-3beta.
CONCLUSIONGinsenoside Rb1 can attenuate beta AP(25-35)-induced tau protein hyperphosphorylation in cortical neurons by inhibiting the expression of GSK-3beta.
