首页> 外文会议>American Peptide Symposium >Cardioprotective Effects of Cell Permeable NADPH Oxidase Inhibitors in Myocardial Isehemia/Reperfusion (I/R) Injury
【24h】

Cardioprotective Effects of Cell Permeable NADPH Oxidase Inhibitors in Myocardial Isehemia/Reperfusion (I/R) Injury

机译:细胞可渗透的NADPH氧化酶抑制剂在心肌肌肉/再灌注(I / R)损伤中的心脏保护作用

获取原文

摘要

In myocardial infarction, reperfusion can compound ischemic damage and cause additional injury. Reperfusion injury is closely related to oxidative stress [1]. Clinical trials suggest nonselective antioxidants do not effectively attenuate reperfusion injury, which may be due to lack of specifically targeting the source of oxidative stress. It is proposed that overproduction of superoxide (SO) by activated NADPH oxidase can serve as a principle source of reactive oxygen species (ROS) under I/R conditions. Overproduction of SO via NADPH oxidase can result in mitochondrial dysfunction, cell/tissue damage, endothelial nitric oxide synthase (eNOS) uncoupling, and vessel constriction [2]. Therefore, we hypothesize that administration of selective NADPH oxidase inhibitors, gp91 ds-tat (RKKRRQRRR-CSTRIRRQL-amide, MW=2452 g/mol, Genemed Synthesis Inc. San Antonio, TX) or apocynin (MW=166 g/mol, Sigma Chemicals), will improve postreperfused cardiac function and reduce infarct size [3,4].
机译:在心肌梗塞中,再灌注可以复合缺血性损伤并导致额外的伤害。再灌注损伤与氧化应激密切相关[1]。临床试验表明非选择性抗氧化剂不会有效地衰减再灌注损伤,这可能是由于缺乏氧化应激来源的缺乏。提出,通过活化的NADPH氧化酶过量生产超氧化物(SO)可以作为I / R条件下的反应性氧物质(ROS)的原理来源。通过NADPH氧化酶过量生产可导致线粒体功能障碍,细胞/组织损伤,内皮损伤,内皮一氧化氮合酶(eNOS)脱胶和血管收缩[2]。因此,我们假设施用选择性NADPH氧化酶抑制剂,GP91 DS-TAT(RKKRRQRRR-CSTRIRRQL-酰胺,MW = 2452g / mol,基因酸合成Inc.SAN Antonio,TX)或Apocynin(MW = 166g / mol,Sigma化学品),将改善PostreperFused心功能并降低梗塞尺寸[3,4]。

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