| Literature DB >> 14741394 |
Wenya Wang1, Leyu Shi, Yuanbin Xie, Chi Ma, Wenming Li, Xingwen Su, Shoujian Huang, Ruzhu Chen, Zhenyu Zhu, Zixu Mao, Yifan Han, Mingtao Li.
Abstract
Increasing evidence suggests that c-Jun N-terminal kinase (JNK) is an important kinase mediating neuronal apoptosis in Parkinson's disease (PD) model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In order to study roles of JNK activity in neuronal apoptosis in this model, we blocked JNK activity in vivo using a specific inhibitor of JNK, SP600125. Our data showed that MPTP-induced phospho-c-Jun of substantial nigral neurons, caused apoptosis of dopaminergic neurons, and decreased the dopamine level in striatal area. We found that inhibiting JNK with SP600125 reduced the levels of c-Jun phosphorylation, protected dopaminergic neurons from apoptosis, and partly restored the level of dopamine in MPTP-induced PD in C57BL/6N mice. These results indicate that JNK pathway is the major mediator of the neurotoxic effects of MPTP in vivo and inhibiting JNK activity may represent a new and effective strategy to treat PD.Entities:
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Year: 2004 PMID： 14741394 DOI： 10.1016/j.neures.2003.10.012
Source DB: PubMed Journal: Neurosci Res ISSN： 0168-0102 Impact factor: 3.304