• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文会议>Triennial Meeting of the International Basal Ganglia Society >Upregulation of NAD(P)H:Quinone Oxidoreductase (NQO1) in Glial Cells of 6-Hydroxydopamine-Lesioned Substantia Nigra in the Rat
【24h】

Upregulation of NAD(P)H:Quinone Oxidoreductase (NQO1) in Glial Cells of 6-Hydroxydopamine-Lesioned Substantia Nigra in the Rat

机译：NAD（P）H：醌氧化还原酶（NQO1）在大鼠6-羟基多胺 - 损伤的胶质细胞中的喹啉氧化还原酶（NQO1）

获取原文
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Dopamine quinone toxicity has been implicated in the degeneration of nigral dopaminergic (DA) neurons in Parkinson's disease (PD). NAD(P)H:quinone oxidoreductase (NQO1) may protect against this quinone toxicity. In Parkinsonian brains, levels of NQO1are increased in reactive glia cells that are located around the remaining DA neurons in the substantia nigra pars compacta (SNc), suggesting a neuroprotective role of NQO1. It is not known at which stage of the disease process the Upregulation of glialNQO1 starts. Furthermore, it is at present not clear whether NQO1 indeed plays a neuroprotective role in the disease process. As a first step to experimentally study a potential neuroprotective role of NQO1, it was examined whether activation of glia cells and changes in the distribution of NQO1-positive glia cells and the expression levels of glial NQO1, as seen in PD brains, also occurred in a 6-hydroxy-dopamine (6-OHDA) rat model of PD. Our results show that astroglia cells and microglia cells were activated. Furthermore, NQO1 was upregulated in astroglia cells in the SNc in those areas in which DA neurons degenerated. The time course and pattern of Upregulation of NQO1 paralleled those of the degeneration of DA neurons. Activated microglia were seen at a later stage during the course of degeneration of DA neurons. In conclusion, in the present model, astroglia cells and microglia cells are activated in response to 6-OHDA-induced oxidative stress. Furthermore, levels of NQO1 are increased in astroglia cells. The findings in the present model are in line with the findings as seen in parkinsonian brains. The 6-OHDA rat model of PD is, therefore, suitable for further research to examine a potential neuroprotective role of NQOl.
机译：多巴胺醌毒性一直涉及帕金森病（Pd）中的八峰多巴胺能（DA）神经元的退化。 NAD（P）H：醌氧化还原酶（NQO1）可以防止这种醌毒性。在Parkinsonian大脑中，位于剩余的Da神经元的反应性胶质细胞中，NQO1的水平增加，该细胞位于Complia Nigra Compara（SNC）中的剩余DA神经元，表明NQO1的神经保护作用。尚不清楚疾病过程的阶段，Glialnqo1的上调开始。此外，目前尚不清楚NQO1是否确实在疾病过程中发挥神经保护作用。作为通过实验研究潜在的NQO1的神经保护作用的第一步，检查了PD大脑中是否存在胶质细胞的激活和NQO1阳性胶质细胞的分布和胶质NQO1的表达水平的激活，如PD大脑中也发生了Pd的6-羟基多巴胺（6-OHDA）大鼠模型。我们的研究结果表明，激活了星形菌龈细胞和微胶质细胞。此外，在SNC中的那些区域中的这些区域中，在SNC中的星形菌细胞中上调，NQO1在其中退化的那些区域。 NQO1平行于Da神经元变性的时间过程和上调模式。在Da神经元的退化过程中，在后期看到活化的微胶质细胞。总之，在本模型中，响应于6-OHDA诱导的氧化应激而激活星形菌龈细胞和微胶质细胞。此外，在星形菌细胞中增加了NQO1的水平。本模型中的发现符合Parkinsonian大脑中所见的研究结果。因此，Pd的6-OHDA大鼠模型适用于进一步研究，以检查NQOL的潜在神经保护作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号