Salidroside Protects Dopaminergic Neurons by Enhancing PINK1/Parkin-Mediated Mitophagy

Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the degeneration of nigrostriatal dopaminergic (DA) neurons. Our previous studies have suggested that salidroside (Sal) might play neuroprotective effects against PD by preserving mitochondrial Complex I activity. Howeve...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-11
Main Authors: Li, Ruru, Chen, Jianzong
Format: Article
Language:English
Subjects:
Animals
Autophagy
Dopamine
Dopaminergic Neurons - metabolism
Glucosides - pharmacology
Glucosides - therapeutic use
Homeostasis
Humans
Kinases
Metabolism
Mice
Mitochondria
Mitophagy
Neurons
Parkinson Disease - drug therapy
Parkinson's disease
Phenols - pharmacology
Phenols - therapeutic use
Rhodiola - chemistry
Studies
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Summary:Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the degeneration of nigrostriatal dopaminergic (DA) neurons. Our previous studies have suggested that salidroside (Sal) might play neuroprotective effects against PD by preserving mitochondrial Complex I activity. However, the exact mechanism of the neuroprotective effect of Sal remains unclear. Growing evidence indicates that PINK1/Parkin-mediated mitophagy is involved in the development of PD. In this study, we investigated whether Sal exerts a neuroprotective effect by modulating PINK1/Parkin-mediated mitophagy. Results showed that Sal alleviated MPTP-induced motor deficits in pole test. Moreover, Sal diminished MPTP-induced degeneration of nigrostriatal DA neurons as evidenced by upregulated TH-positive neurons in the substantia nigra, increased DAT expression, and high dopamine and metabolite levels in the striatum. Furthermore, in comparison with the MPP+/MPTP group, Sal considerably increased the mitophagosome and mitophagy flux. Moreover, in comparison with the MPP+/MPTP group, Sal evidently enhanced the mitochondrial expression of PINK1 and Parkin, accompanied by an increase in the colocalization of mitochondria with Parkin. However, transfection of MN9D cells with PINK1 siRNA reversed Sal-induced activated mitophagy and cytoprotective effect. In conclusion, Sal may confer neuroprotective effects by enhancing PINK1/Parkin-mediated mitophagy in MPP+/MPTP-induced PD models.
ISSN:1942-0900
1942-0994
1942-0994
DOI:10.1155/2019/9341018