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Kynurenic acid attenuates MPP+-induced dopaminergic neuronal cell death via a Bax-mediated mitochondrial pathway

Authors
Lee, Do YeonLee, Kyu-SunLee, Hyun JungNoh, Yoo HunKim, Do HeeLee, Jun YoungCho, Soo HyunYoon, Ok JaLee, Won BokKim, Kyung YongChung, Yoon HeeKim, Sung Su
Issue Date
Jun-2008
Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
Keywords
kynurenic acid (KYNA); 1-methyl-4-phenylpyridinium (MPP+); Bax; mitochondrial dysfunction; neuronal apoptosis
Citation
EUROPEAN JOURNAL OF CELL BIOLOGY, v.87, no.6, pp 389 - 397
Pages
9
Journal Title
EUROPEAN JOURNAL OF CELL BIOLOGY
Volume
87
Number
6
Start Page
389
End Page
397
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23739
DOI
10.1016/j.ejcb.2008.03.003
ISSN
0171-9335
1618-1298
Abstract
Kynurenic acid (KYNA), a tryptophan metabolite in the kynurenine pathway, is protective against various insults. However, the molecular mechanism of this protective effect has not been identified. In this study, we examined the protective effects of KYNA against 1-methyl-4-phenylpyridinium (MPP+), the best-characterized toxin inducing pathological changes resembling Parkinson's disease (PD), using SH-SY5Y and SK-N-SH human neuroblastoma cells. Pre-treatment of KYNA attenuated MPP+-induced neuronal cell death in SH-SY5Y and SK-N-SH cells. MPP+-induced cell death was preceded by increases in Bax expression and mitochondrial dysfunction, such as collapse of mitochondrial membrane potential (Delta Psi(m)), release of cytochrome c from mitochondria into the cytoplasm, and increases in caspase-9/-3 activities. KYNA effectively inhibited all of these mitochondrial apoptotic processes. Our results indicate that KYNA plays a protective role by down-regulating Bax expression and maintaining mitochondrial function in MPP+-induced neuronal cell death, and suggest that KYNA may have therapeutic potential in PD. (C) 2008 Elsevier GmbH. All rights reserved.
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