• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>RSC Advances >Teneligliptin protects against ischemia/reperfusion-induced endothelial permeability in vivo and in vitro
【24h】

Teneligliptin protects against ischemia/reperfusion-induced endothelial permeability in vivo and in vitro

机译：Teneligliptin保护体内和体外缺血/再灌注诱导的内皮渗透性

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 stroke is a leading cause of disability and mortality worldwide, especially among the elderly population. Ischemia and reperfusion cause damage to cells and initiate an acute inflammatory response, which leads to cerebral endothelial dysfunction, increased endothelial permeability, and potentially permanent disability. Teneligliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor that has been used almost exclusively in the treatment of type 2 diabetes mellitus. However, it is still unknown whether teneligliptin possesses a protective effect in brain endothelial dysfunction in the context of ischemic stroke. In the present work, we demonstrate the potential of teneligliptin treatment to protect against ischemia/reperfusion-induced damage using a series of both in vivo and in vitro experiments. Our key findings are that administration of teneligliptin could reduce brain infarct volume, ameliorate neurological damage, and improve brain permeability by increasing the expression of the tight junction protein occludin in middle cerebral artery occlusion (MCAO) mice models. Importantly, teneligliptin displayed a robust protective effect against oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell death of primary human brain microvascular endothelial cells (HBMVECs) in vitro. Notably, teneligliptin prevented OGD/R-induced increased endothelial monolayer permeability in HBMVECs by increasing the expression of occludin, which was mediated by the ERK5/KLF2 signaling pathway. These findings suggest that teneligliptin might serve as a potential therapeutic agent for the treatment of stroke
机译：缺血性中风是导致残疾和死亡全世界的主要原因，特别是在老年人群。缺血和再灌注细胞造成损害，并启动急性炎症反应，从而导致脑内皮功能障碍，增加的内皮通透性，和潜在的永久的残疾。特力利汀是已经几乎完全使用在2型糖尿病的治疗中具有二肽基肽-4（DPP-4）抑制剂。但是，它仍然是未知是否特力利汀具有脑血管内皮功能的缺血性中风的情况下有保护作用。在目前的工作中，我们证明特力利汀治疗的潜在的体内和体外实验使用一系列两者，以防止缺血/再灌注引起的损伤。我们的主要发现是特力利汀的施用可以减少脑梗塞体积，改善神经功能的损伤，并且通过在大脑中动脉闭塞（MCAO）模型小鼠增加紧密连接蛋白的表达，闭合蛋白改善脑渗透性。重要的是，特力利汀显示对氧气 - 葡萄糖剥夺鲁棒保护作用/再灌注（OGD / R）体外原代人脑微血管内皮细胞（HBMVECs）的诱导的细胞死亡。值得注意的是，特力利汀防止OGD / R诱导的通过增加occludin的，这是由ERK5 / KLF2信号通路介导的表达增加HBMVECs内皮细胞单层渗透性。这些发现表明，特力利汀可能作为治疗中风的潜在治疗剂

著录项

  • 来源
    《RSC Advances》 |2020年第7期|共10页
  • 作者

    Zhang Lei; Yuan Weiqiong; Kong Xiangli; Zhang Bei;

  • 作者单位

    Xian Med Univ Affiliated Hosp 1 Dept Neurol 48 Fenghao West Rd Xian Shaanxi Peoples R China;

    Xi An Jiao Tong Univ Affiliated Hosp 2 Dept Gen Surg Xian Shaanxi Peoples R China;

    Xian Med Univ Affiliated Hosp 1 Dept Neurol 48 Fenghao West Rd Xian Shaanxi Peoples R China;

    Xian Med Univ Affiliated Hosp 1 Dept Neurol 48 Fenghao West Rd Xian Shaanxi Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
  • 关键词

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