Bystrom Phillip, Foley Nicole, Toledo-Pereyra Luis, Quesnelle Kelly
Western Michigan University, Homer Stryker M.D. School of Medicine Department of Biomedical Sciences.
Western Michigan University, Homer Stryker M.D. School of Medicine Department of Surgery.
EXCLI J. 2017 Apr 7;16:483-496. doi: 10.17179/excli2017-166. eCollection 2017.
Ischemia reperfusion (IR) injury is a significant cause of morbidity and mortality in liver transplantation. When oxygen is reintroduced to the liver graft it initiates a cascade of molecular reactions leading to the release of reactive oxygen species (ROS) and pro-inflammatory cytokines. These soluble mediators propagate a sterile immune response to cause significant tissue damage. Ischemic preconditioning (IPC) is one method that reduces hepatocellular injury by altering the immune response and inhibiting the production of ROS. Studies quantifying the effects of IPC in humans have demonstrated an improved liver enzyme panel in patients receiving grafts pretreated with IPC as compared to patients receiving the standard of care. In our review, we explore current literature in the field in order to describe the mechanism through which IPC regulates the production of ROS and improves IR injury.
缺血再灌注（IR）损伤是肝移植中发病和死亡的重要原因。当向肝移植物重新供氧时，会引发一系列分子反应，导致活性氧（ROS）和促炎细胞因子的释放。这些可溶性介质引发无菌免疫反应，造成显著的组织损伤。缺血预处理（IPC）是一种通过改变免疫反应和抑制ROS产生来减轻肝细胞损伤的方法。量化IPC对人类影响的研究表明，与接受标准治疗的患者相比，接受IPC预处理移植物的患者肝功能酶指标有所改善。在我们的综述中，我们探索了该领域的现有文献，以描述IPC调节ROS产生并改善IR损伤的机制。
