- Author:
Linhui LIANG
1
;
Yingcheng WANG
;
Jinxue WEI
;
Xiaochu GU
;
Bo XIANG
;
Xiaohong MA
;
Tao LI
Author Information
- Publication Type:Journal Article
- MeSH: Antipsychotic Agents; pharmacology; Cell Line, Tumor; Glioma; drug therapy; genetics; metabolism; Glycogen Synthase Kinase 3; genetics; metabolism; Glycogen Synthase Kinase 3 beta; Humans; Phosphatidylinositol 3-Kinases; genetics; metabolism; Phosphorylation; Proto-Oncogene Proteins c-akt; genetics; metabolism; Risperidone; pharmacology; Signal Transduction; drug effects
- From: Chinese Journal of Medical Genetics 2014;31(6):693-697
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of risperidone, an antipsychotic drug, on the Akt-GSK3β pathway and the role of PI3K in dopamine D2 receptor (DRD2) expression and Akt-GSK3β signal pathway.
METHODSHuman glioma cells (U251) were cultured in vitro. Cells without any treatment as control, Western blotting was used for measuring the expression of Akt (Thr308 and Ser473) and GSK3β (Ser9) protein phosphorylation by risperidone and LY294002 in U251 cell, and real-time PCR was used for detecting the expression of DRD2 mRNA.
RESULTSRisperidone has significantly enhanced the expression of phosphorylated Akt and phosphorylated GSK3β (P< 0.05), but did not alter the mRNA expression of DRD2. LY294002 could reduce the phosphorylation of Akt and GSK3β (P< 0.01, P< 0.05), and also decrease the DRD2 mRNA (P<0 .05).
CONCLUSIONRisperidone can activate the Akt-GSK3β signaling pathway in the U251 cells, and PI3K is a common regulatory site in Akt-GSK3β signaling and D2 receptor gene expression.