Deng Xin, Ouyang Peng, Xu Wei, Yang Erhua, Bao Zhen, Wu Yijing, Gong Jin, Pan Jinghua
Division 2, Gastrointestinal Surgery, First Affiliated Hospital of Jinan University, Guangzhou, China.
Front Pharmacol. 2023 Jan 4;13:1103483. doi: 10.3389/fphar.2022.1103483. eCollection 2022.
Hepatic ischemia-reperfusion injury (HIRI) is an additional injury to ischemic tissue after hepatic revascularization, and its pathological mechanism is complex. HIRI is not only involved in the molecular targets that mediate cell death, such as ion channel activation, abnormal protease activation and mitochondrial dysfunction, but also related to the down-regulation of endogenous protective signals. As a by-product of normal aerobic metabolism, reactive oxygen species (ROS) act as a multi effect physiological signal factor at low concentration. However, liver ischemia-reperfusion will lead to excessive ROS accumulation, destroy redox homeostasis, lead to oxidative stress, cause cell death through a variety of mechanisms, and drive the further damage of ischemic liver. Recent studies have found that the antioxidant treatment of nano selenium can reduce the excessive production of ROS and play a potential protective role in reducing HIRI. This paper reviews the molecular mechanism of the antioxidant effect of nano selenium for the prevention and treatment of HIRI, in order to provide further experimental basis for the clinical prevention and treatment of HIRI.
肝缺血再灌注损伤（HIRI）是肝脏血管再通后对缺血组织的一种额外损伤，其病理机制复杂。HIRI不仅涉及介导细胞死亡的分子靶点，如离子通道激活、异常蛋白酶激活和线粒体功能障碍，还与内源性保护信号的下调有关。作为正常有氧代谢的副产物，活性氧（ROS）在低浓度时作为一种多效生理信号因子发挥作用。然而，肝脏缺血再灌注会导致ROS过度积累，破坏氧化还原稳态，导致氧化应激，通过多种机制引起细胞死亡，并促使缺血肝脏进一步损伤。最近的研究发现，纳米硒的抗氧化治疗可以减少ROS的过量产生，并在减轻HIRI方面发挥潜在的保护作用。本文综述了纳米硒抗氧化作用预防和治疗HIRI的分子机制，以期为HIRI的临床防治提供进一步的实验依据。
