6-hydroxydopamine-induced nuclear factor-kappaB activation in PC12 cells

被引:39
作者
Blum, D
Torch, S
Nissou, MF
Verna, JM
机构
[1] ULB Erasme, Dept Neurosci, Neurophysiol Lab, B-1070 Brussels, Belgium
[2] CHU Michallon, INSERM, Equipe Mixte, F-38043 Grenoble 9, France
[3] Immunol Lab, F-38130 Echirolles, France
关键词
NF-kappaB; PC12; cells; 6-hydroxydopamine; bcl-2; Parkinson's disease;
D O I
10.1016/S0006-2952(01)00680-3
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The involvement of nuclear Factor-kappaB (NF-kappaB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-kappaB. When the NF-kappaB activation was inhibited by parthenolide, PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-kappaB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1. Although Bcl-2 and Bfl-1 expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-kappaB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-kappaB activation. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:473 / 481
页数:9
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