MPP+ decreased BDNF expression in PC12 cells.
- Author:
Yu-he YUAN
1
;
Jian-dong SUN
;
Jin-feng HU
;
Nai-hong CHEN
Author Information
1. Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- MeSH:
1-Methyl-4-phenylpyridinium;
administration & dosage;
pharmacology;
Animals;
Brain-Derived Neurotrophic Factor;
metabolism;
Calcium-Calmodulin-Dependent Protein Kinase Type 2;
metabolism;
Cell Survival;
drug effects;
Cyclic AMP Response Element-Binding Protein;
drug effects;
Dose-Response Relationship, Drug;
Extracellular Signal-Regulated MAP Kinases;
drug effects;
PC12 Cells;
Phosphorylation;
Rats;
Signal Transduction
- From:
Acta Pharmaceutica Sinica
2009;44(4):362-365
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study is to investigate the neurotoxic effect and mechanism of 1-methyl-4-phenylpyridinium (MPP+) on PC12 cells. MTT assay was used to investigate cell viability, Western blotting assay was performed to observe the protein level and phosphorylation, and dual-luciferase assay was used to study the transactivation. The experiment showed that MPP+ could decrease cell viability significantly in a dose-dependent manner and could decrease BDNF protein level, depress the phosphorylation of ERK, and attenuate the phosphorylation and transactivation of CREB, which is one of transcription factors of BDNF, but did not affect the activity of CaMK II in PC12 cells. So MPP+ might decrease BDNF protein level through MAPK/ERK signal pathway.
