[Protective effect of edaravone on balance of mitochondrial fusion and fission in MPP+-treated PC12 cells].
[Protective effect of edaravone on balance of mitochondrial fusion and fission in MPP+-treated PC12 cells].
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Xuzhou, CN · Author affiliation
The 71st Group Military Hospital of the Chinese People's Liberation Army, Xuzhou 221004, China.Location evidence
Nanjing, CN · Author affiliation
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing 210029, China.Location evidence
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Original 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.