Protective effect of edaravone on balance of mitochondrial fusion and fission in MPP-treated PC12 cells.
- Author:
Yang JIAO
1
;
Yue ZHENG
2
;
Cheng-Jie SONG
3
Author Information
1. The 71st Group Military Hospital of the Chinese People's Liberation Army, Xuzhou 221004, China.
2. Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing 210029, China.
3. Department of Physiology, Xuzhou Medical University, Xuzhou 221004, China. songcj09@xzhmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
1-Methyl-4-phenylpyridinium;
Animals;
Dynamins;
Edaravone;
pharmacology;
GTP Phosphohydrolases;
Mitochondria;
drug effects;
Mitochondrial Dynamics;
Mitochondrial Proteins;
PC12 Cells;
Parkinson Disease;
Rats;
Up-Regulation
- From:
Acta Physiologica Sinica
2020;72(2):249-254
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the effect of edaravone (Eda) on the balance of mitochondrial fusion and fission in Parkinson's disease (PD) cell model. A cell model of PD was established by treating PC12 cells with 500 μmol/L 1-methyl-4-phenylpyridinium (MPP). Thiazole blue colorimetry (MTT) was used to detect the effect of different concentrations of Eda on the survival rate of PC12 cells exposed to MPP. The mitochondrial morphology was determined by laser confocal microscope. Western blot was used to measure the protein expression levels of mitochondrial fusion- and fission-related proteins, including OPA1, MFN2, DRP1 and Fis1. The results showed that pretreatment with different concentrations of Eda antagonized MPP-induced PC12 cell damage in a dose-dependent manner. The PC12 cells treated with MPP showed mitochondrial fragmentation, up-regulated DRP1 and Fis1 protein expression levels, and down-regulated MFN2 and OPA1 protein expression levels. Eda could reverse the above changes in the MPP-treated PC12 cells, but did not affect Fis1 protein expression. These results suggest that Eda has a protective effect on the mitochondrial fusion disruption induced by MPP in PC12 cells. The mechanism may be related to the up-regulation of OPA1/MFN2 and down-regulation of DRP1.
