• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Differential effects of COX inhibitors against beta-amyloid-induced neurotoxicity in human neuroblastoma cells.
【24h】

Differential effects of COX inhibitors against beta-amyloid-induced neurotoxicity in human neuroblastoma cells.

机译：COX抑制剂对人成神经细胞瘤细胞中β淀粉样蛋白诱导的神经毒性的不同作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Retrospective epidemiological studies have suggested that chronic treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) provides some degree of protection from Alzheimer's disease (AD). Although most NSAIDs inhibit the activity of cyclooxygenase (COX), the rate-limiting enzyme in the production of prostanoids from arachidonic acid (AA), the precise mechanism through which NSAIDs act upon AD pathology remains to be elucidated. Classical NSAIDs like indomethacin inhibit both the constitutive COX-1 and the inducible COX-2 enzymes. In the present work, we characterize the protective effect of the indomethacin on the neurotoxicity elicited by amyloid-beta protein (A beta, fragments 25-35 and 1-42) alone or in combination with AA added exogenously as well as its effects on COX-2 expression. We also compared the neuroprotective effects of indomethacin with the selective COX-1, COX-2 and 5-LOX inhibitors, SC-560, NS-398 and NDGA, respectively. Our results show that indomethacin protected from A beta andAA toxicity in naive and differentiated human neuroblastoma cells with more potency than SC-560 while, NS-398 only protected neurons from AA-mediated toxicity. Present results suggest that A beta toxicity can be reversed more efficiently by the non-selective COX inhibitor indomethacin suggesting its role in modulating the signal transduction pathway involved in the mechanism of A beta neurotoxicity.
机译：回顾性流行病学研究表明，使用非甾体抗炎药（NSAIDs）进行的长期治疗可提供一定程度的针对阿尔茨海默氏病（AD）的保护。尽管大多数NSAID抑制了环氧合酶（COX）的活性，环氧合酶是花生四烯酸（AA）生产类前列腺素中的限速酶，但NSAID对AD病理作用的确切机制尚待阐明。经典的NSAID（如吲哚美辛）抑制组成型COX-1和诱导型COX-2酶。在目前的工作中，我们表征了吲哚美辛对单独或与外源添加AA的淀粉样β蛋白（Aβ，片段25-35和1-42）引起的神经毒性的保护作用及其对COX的影响-2表达式。我们还比较了吲哚美辛与选择性COX-1，COX-2和5-LOX抑制剂SC-560，NS-398和NDGA的神经保护作用。我们的结果表明，吲哚美辛在幼稚和分化的人类神经母细胞瘤细胞中具有保护作用，使其免受A beta和AA毒性的侵害，其作用力比SC-560强，而NS-398仅保护神经元免受AA介导的毒性作用。目前的结果表明，非选择性COX抑制剂吲哚美辛可以更有效地逆转Aβ毒性，表明其在调节参与Aβ神经毒性机制的信号转导途径中的作用。

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