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 (DeltaPsi(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.
journal_name
Eur J Cell Bioljournal_title
European journal of cell biologyauthors
Lee DY,Lee KS,Lee HJ,Noh YH,Kim DH,Lee JY,Cho SH,Yoon OJ,Lee WB,Kim KY,Chung YH,Kim SSdoi
10.1016/j.ejcb.2008.03.003subject
Has Abstractpub_date
2008-06-01 00:00:00pages
389-97issue
6eissn
0171-9335issn
1618-1298pii
S0171-9335(08)00061-7journal_volume
87pub_type
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journal_title:European journal of cell biology
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