Volume 458, Issue 2, 6 March 2015, Pages 227–233
- Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, 569 Xinsi Road, Xi'an, Shaanxi 710038, China
- Received 31 December 2014, Available online 23 January 2015
Highlights
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- Myricitrin prevented a MPP+-induced reduction in cell viability in SN4741 cells.
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- Myricitrin effectively rescued DJ-1 from MPP+-induced decline in SN4741 cells.
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- Myricitrin rescued mitochondrial dysfunction in a DJ-1-dependent manner.
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- Myricitrin attenuated MPP+-induced cellular death by preventing mitochondrial dysfunction in a DJ-1-dependent manner.
Abstract
Oxidative
stress and mitochondrial dysfunction have been linked to Parkinson's
disease. DJ-1 is a recessive familial PD gene involved in antioxidative
function and mitochondrial maintenance. Myricitrin, a flavanoid isolated
from the root bark of Myrica cerifera, has potent antioxidative properties. In the present study, we investigated the protective effects of myricitrin against MPP+-induced
mitochondrial dysfunction in SN4741 cells and attempted to elucidate
the mechanisms underlying this protection. The results showed that
incubating SN4741 cells with myricitrin significantly reduced cell death
induced by the neurotoxin MPP+. Furthermore, myricitrin protected cells from MPP+-induced
effects on mitochondrial morphology and function. However, these
protective effects were lost under DJ-1-deficient conditions. Thus, our
results suggest that myricitrin alleviates MPP+-induced
mitochondrial dysfunction and increases cell viability via DJ-1,
indicating that myricitrin is a potential beneficial agent for
age-related neurodegenerative diseases, particularly Parkinson's
disease.
Keywords
- Parkinson's disease;
- Myricitrin;
- Mitochondria;
- DJ-1;
- Neuronal death
Abbreviations
- Myr, myricitrin;
- MPP+, 1-methyl-4-phenylpyridinium;
- PD, Parkinson's disease;
- MMP, mitochondrial membrane potential
Copyright © 2015 Elsevier Inc. All rights reserved.
