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

被引:40
作者
Bae, Woom-Yee [1 ]
Choi, Jae-Sun [2 ]
Jeong, Joo-Won [1 ,2 ]
机构
[1] Kyung Hee Univ, Grad Sch, Dept Biomed Sci, Seoul 02447, South Korea
[2] Kyung Hee Univ, Dept Anat & Neurobiol, Coll Med, Seoul 02447, South Korea
基金
新加坡国家研究基金会;
关键词
cinnamic aldehyde; autophagy; Parkinson's disease; MPTP; MPP+; CELL-DEATH; CDK5-MEDIATED PHOSPHORYLATION; TRANS-CINNAMALDEHYDE; OXIDATIVE STRESS; AUTOPHAGY; NEURODEGENERATION; DYSFUNCTION; APOPTOSIS; BRAIN; DRUGS;
D O I
10.3390/ijms19020551
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
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页数:10
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