• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>International Journal of General Medicine >Some mechanisms of the protective effect of ischemic preconditioning on rat liver ischemia-reperfusion injury
【24h】

Some mechanisms of the protective effect of ischemic preconditioning on rat liver ischemia-reperfusion injury

机译：缺血预处理对大鼠肝脏缺血再灌注损伤保护作用的某些机制

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract: Ischemia-reperfusion (I/R) injury is a multifactorial process that affects graft function after liver transplantation. An understanding of the mechanisms involved in I/R injury is essential for the design of therapeutic strategies to improve the outcome of liver transplantation. The generation of reactive oxygen species subsequent to reoxygenation inflicts tissue damage and initiates a cascade of deleterious cellular responses, leading to inflammation, cell death, and ultimate organ failure. Increasing experimental evidence has suggested that Kupffer cells and T-cells mediate activation of neutrophil inflammatory responses. Activated neutrophils infiltrate the injured liver in parallel with increased expression of adhesion molecules on endothelial cells. The heme oxygenase system is among the most critical of the cytoprotective mechanisms activated during cellular stress, exerting antioxidant and anti-inflammatory functions, modulating the cell cycle, and maintaining the microcirculation. Finally, the activation of toll-like receptors on Kupffer cells may play a fundamental role in exploring new therapeutic strategies based on the concept that hepatic I/R injury represents a case for host “innate” immunity. In the present study, there was a significant decrease in hepatic activity of glycogen in the I/R group as compared with corresponding values in the control group. On the other hand, there was a significant increase in the hepatic activity of glycogen in the I/R-IP (ischemic preconditioning) group as compared with corresponding values in the I/R group.
机译：摘要：缺血再灌注（I / R）损伤是影响肝移植后移植物功能的多因素过程。对I / R损伤所涉及的机制的了解对于设计改善肝移植结局的治疗策略至关重要。复氧后活性氧的产生会破坏组织并引发一系列有害的细胞反应，从而导致炎症，细胞死亡和最终器官衰竭。越来越多的实验证据表明，枯否细胞和T细胞介导嗜中性粒细胞炎症反应的激活。活化的中性粒细胞与内皮细胞上粘附分子表达的增加并行地渗入受伤的肝脏。血红素加氧酶系统是在细胞应激过程中激活，发挥抗氧化剂和抗炎功能，调节细胞周期并维持微循环的最关键的细胞保护机制之一。最后，基于肝I / R损伤代表宿主“先天”免疫的概念，库普弗细胞上Toll样受体的激活可能在探索新的治疗策略中起重要作用。在本研究中，与对照组相比，I / R组肝糖原的肝活动显着降低。另一方面，与I / R组中的相应值相比，I / R-IP（缺血预处理）组中糖原的肝活性显着增加。

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