• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Anti-tussive and bronchodilator mechanisms of action for the enaminone E121.
【24h】

Anti-tussive and bronchodilator mechanisms of action for the enaminone E121.

机译：酶E121的抗追求和支气管扩张剂的作用机制。

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

AIMS: In this study, we investigated whether the enaminone, E121, has anti-tussive effects in a guinea pig model of cough, and if so, whether this effect is mediated via a central or peripheral site of action. We also assessed whether E121 has bronchodilator effects and the molecular mechanisms underlying any anti-tussive and/or bronchodilator effects. MAIN METHODS: Whole body plethysmography was used to assess both cough and airway obstruction. A stereotaxic apparatus was used to administer drugs intracerebroventricularly (i.c.v.). Effects of E121 were examined in vitro on contractile effects in guinea pig bronchioles. KEY FINDINGS: Pre-treatment of animals with E121 resulted in a significant inhibition in the citric acid-induced cough and airway obstruction compared to vehicle-pretreated animals. The K(ATP) antagonist, glibenclamide, significantly inhibited the anti-tussive and bronchoprotective effects of E121. Also, intra-tracheal administration of E121 resulted in a significant inhibition of both the citric acid-induced cough response and airway obstruction compared to vehicle-pretreated animals. By contrast, i.c.v. administration had no effect. Finally, E121 significantly inhibited carbachol-induced airway smooth muscle contractions, an effect that was reduced by both glibenclamide and propranolol. Interestingly, E121 enhanced histamine-induced cAMP release in human eosinophils although it did not directly elevate cAMP levels. SIGNIFICANCE: The enaminone, E121, has anti-tussive and bronchodilatory effects and is topically, but not centrally, active. The anti-tussive mechanism of action of E121 seems to be K(ATP) channel dependent, whereas its bronchodilatory effects appear to be mediated via activation of both K(ATP) channels and beta(2) receptors. Therefore, E121 may potentially represent a novel therapy for cough, particularly cough associated with airway obstruction.
机译：目的：在这项研究中，我们研究了酶，E121是否对咳嗽的豚鼠模型具有反致服作用，如果是的话，是否通过中央或外围部位介导的这种效果。我们还评估了E121是否具有支气管扩张剂效应和潜在的任何抗疑究和/或支气管扩张剂效应的分子机制。主要方法：全身体积描绘用于评估咳嗽和气道阻塞。使用立体岩装置给脑内（I.C.V.）给药药物。在豚鼠支气管中的收缩效应上检查了E121的影响。主要发现：与E121的动物预处理导致柠檬酸诱导的咳嗽和气道阻塞的显着抑制与载体预处理动物相比。 K（ATP）拮抗剂Glibenclamide显着抑制了E121的抗脑子和支气管扩张作用。此外，与载体预处理动物相比，气管内施用E121导致柠檬酸诱导的咳嗽响应和气道梗阻的显着抑制。相比之下，I.C.V.政府没有效果。最后，E121显着抑制了碳酰酚诱导的气道平滑肌收缩，这是Glibenclamide和普萘洛尔减少的效果。有趣的是，E121增强了组胺诱导的人类嗜酸性粒细胞中的露营释放，尽管它​​没有直接提升CAMP水平。意义：酶，E121，具有反致力的和支气管扩张效果，局部，但不是集中，活跃。 E121的抗疑究机制似乎是K（ATP）通道依赖性，而其支气管扩张效果似乎通过激活K（ATP）通道和β（2）受体来介导。因此，E121可能代表咳嗽的新疗法，特别是与气道阻塞相关的咳嗽。

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