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Title 

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

Authors 

D Y LeeKyu-Sun LeeH J LeeY H NohD H KimJ Y LeeS H ChoO J YoonW B LeeK Y KimY H ChungS S Kim

Publisher 

Elsevier

Issue Date 

2008

Citation 

European Journal of Cell Biology, vol. 87, no. 6, pp. 389-397

Keywords 

1-methyl-4-phenylpyridinium (MPP+)baxmitochondrial dysfunctionneuronal apoptosiscaspase 3caspase 9kynurenic acidprotein Baxapoptosisbrain mitochondrion

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 (ΔΨm), 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.

ISSN 

0171-9335

Link 

http://dx.doi.org/10.1016/j.ejcb.2008.03.003

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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