• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Elevated semicarbazide-sensitive amine oxidase (SSAO) activity in lung with ischemia-reperfusion injury: Protective effect of ischemic preconditioning plus SSAO inhibition
【24h】

Elevated semicarbazide-sensitive amine oxidase (SSAO) activity in lung with ischemia-reperfusion injury: Protective effect of ischemic preconditioning plus SSAO inhibition

机译：肺缺血/再灌注损伤中氨基脲敏感的胺氧化酶（SSAO）活性升高：缺血预处理和SSAO抑制作用的保护作用

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

Ischemic preconditioning (IP) has been shown to protect the lung against ischemia-reperfusion (I/R) injury. Although the production of reactive oxygen species (ROS) has been postulated to play a crucial role in LIR injury, the sources of these radicals in I/R and the mechanisms of protection in IP remain unknown. Since it was postulated that deamination of endogenous and exogenous amines by semicarbazide-sensitive amine oxidase (SSAO) in tissue damage leads to the overproduction of hydrogen peroxide (H2O2), we investigated the possible contribution of tissue SSAO to excess ROS generation and lipid peroxidation during I/R and IP of the lung. Male Wistar rats were randomized into 6 groups: control lungs were subjected to 30 min of perfusion in absence and presence of SSAO inhibitor, whereas the lungs of the I/R group were subjected to 2 h of cold ischemia following the 30 min of perfusion in absence and presence of SSAO inhibitor. IP was performed by two cycles of 5 min ischemia followed by 5 min of reperfusion prior to 2 h of hypothermic ischemia in absence and presence of SSAO inhibitor. Lipid peroxidation, reduced (GSH) and oxidized (GSSG) glutathione levels, antioxidant enzyme activities, SSAO activity, and H2O2 release were determined in tissue samples of the study groups. Lipid peroxidation, glutathione disulfide (GSSG) content, SSAO activity and H2O, release were increased in the I/R group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were decreased. SSAO activity, H2O2 release, GSSG content and lipid peroxidation were markedly decreased in the IP group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were significantly increased. SSAO activity was found to be positively correlated with H2O2 production in all study groups. Increased lipid peroxidation, SSAO activity, GSSG and H2O2 contents as well as decreased GSH and antioxidant enzyme levels in I/R returned to their basal levels when IP and SSAO inhibition were applied together. The present study suggests that application of I P and SSAO inhibition together may be more effective than IP alone against I/R injury in the lung. (c) 2005 Elsevier Inc. All rights reserved.
机译：缺血预处理（IP）已显示可保护肺免受缺血再灌注（I / R）损伤。尽管已经假定活性氧（ROS）的产生在LIR损伤中起关键作用，但I / R中这些自由基的来源以及IP中的保护机制仍然未知。由于据推测，氨基脲敏感的胺氧化酶（SSAO）在组织损伤中对内源性胺和外源性胺的脱氨基作用会导致过氧化氢（H2O2）的过量产生，因此我们研究了组织SSAO对过氧化氢生成和脂质过氧化的可能贡献肺的I / R和IP。将Wistar雄性大鼠随机分为6组：在不存在和存在SSAO抑制剂的情况下，对对照肺进行30分钟的灌注，而对I / R组的肺在30min灌注后进行2h的冷缺血。是否存在SSAO抑制剂。在不存在和存在SSAO抑制剂的情况下，通过2个5分钟的缺血再注入5分钟的再灌注过程进行IP，然后进行2小时的低温缺血。在研究组的组织样本中确定了脂质过氧化，还原型（GSH）和氧化型（GSSG）谷胱甘肽水平，抗氧化酶活性，SSAO活性和H2O2释放。 I / R组脂质过氧化，谷胱甘肽二硫（GSSG）含量，SSAO活性和H2O释放增加，而GSH含量，GSH / GSSG比和抗氧化酶活性下降。 IP组SSAO活性，H2O2释放，GSSG含量和脂质过氧化作用明显降低，而GSH含量，GSH / GSSG比和抗氧化酶活性显着增加。在所有研究组中，SSAO活性均与H2O2的产生呈正相关。当同时应用IP和SSAO抑制作用时，脂质过氧化作用增加，SSAO活性，GSSG和H2O2含量增加，I / R中GSH和抗氧化酶含量降低，恢复到基础水平。本研究表明，I P和SSAO抑制的联合应用可能比单独IP对肺I / R损伤更有效。 （c）2005 Elsevier Inc.保留所有权利。

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