The Neuroprotective Effects of Cinnamic Aldehyde in an MPTP Mouse Model of Parkinson's Disease

Cinnamic aldehyde (CA), a key flavor compound in cinnamon essential oil, has been identified as an anti-oxidant, anti-angiogenic, and anti-inflammatory material. Recently, the neuroprotective effects of CA have been reported in various neurodegenerative disorders, including Parkinson's disease...

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Bibliographic Details
Published in:International journal of molecular sciences 2018-02, Vol.19 (2), p.551
Main Authors: Bae, Woom-Yee, Choi, Jae-Sun, Jeong, Joo-Won
Format: Article
Language:English
Subjects:
Acrolein - analogs & derivatives
Acrolein - pharmacology
Acrolein - therapeutic use
Angiogenesis
Animal models
Animals
Antioxidants
Autophagy
Cell Line, Tumor
cinnamic aldehyde
Cinnamon
Dopamine receptors
Essential oils
Flavor
Humans
Inflammation
Male
Mice
Mice, Inbred C57BL
Microtubule-Associated Proteins - metabolism
MPP
MPTP
MPTP Poisoning - drug therapy
Neurodegeneration
Neurons - drug effects
Neurons - metabolism
Neuroprotection
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Parkinson's disease
Phagocytosis
Substantia nigra
Substantia Nigra - cytology
Substantia Nigra - drug effects
Substantia Nigra - metabolism
Therapeutic applications
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Summary:Cinnamic aldehyde (CA), a key flavor compound in cinnamon essential oil, has been identified as an anti-oxidant, anti-angiogenic, and anti-inflammatory material. Recently, the neuroprotective effects of CA have been reported in various neurodegenerative disorders, including Parkinson's disease (PD). In neurons, autophagy is tightly regulated, and consequently, the dysregulation of autophagy may induce neurodegenerative disorders. In the present study, we found that the selective dopaminergic neuronal death in the substantia nigra of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse models was prevented by CA. Stimulation of microtubule-associated protein light chain 3 (LC3) puncta mediated by MPTP treatment was decreased by CA. Moreover, down-regulated p62 in the substantia nigra of MPTP mice was increased by administration of CA. Finally, we showed that blockage of autophagy using autophagy inhibitors protected the 1-methyl-4-phenylpyridinium (MPP⁺)-mediated death of BE(2)-M17 cells. Together these results suggest that CA has a neuroprotective effect in a PD model and that inhibition of autophagy might be a promising therapeutic target for PD.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms19020551