肝移植术后肝缺血再灌注损伤保护作用的研究进展

Research progress on protective effect of liver ischemia-reperfusion injury after liver transplantation

肝缺血再灌注损伤是肝移植术后最常见的并发症。活性氧生成过多导致的氧化应激、自噬、炎症反应是造成肝缺血再灌注损伤的重要步骤。其中,核转录因子红系2相关因子2被认为是抗氧化反应的主要调节因子,PI3K-Akt-mTOR通路被认为是自噬的重要通路,HMGB1-TLR4-NF-κB通路被认为是导致炎症的关键信号通路,本文将从上述通路及调节分子出发,分别从基因、分子、药物等方面研究对肝缺血再灌注细胞的抗氧化、抗炎、调节自噬作用,探究对肝缺血再灌注细胞的保护作用。

Hepatic ischemia-reperfusion injury is the most common complication after liver transplantation.Oxidative stress,autophagy,and inflammatory response caused by excessive reactive oxygen species production are significant steps that cause liver ischemia-reperfusion injury.What′s more,nuclear factor erythroid 2-related factor 2 is considered to be a major regulator of the antioxidant response,the PI3K-Akt-mTOR signaling pathway is considered to be an important pathway of autophagy,and the HMGB1-TLR4-NF-κB signaling pathway is considered to be a key signaling pathway which leads to inflammation.Based on the above signaling pathways and regulatory factor,this article shows that the antioxidant,anti-inflammatory and autophagy regulation effects of genes,molecules and drugs on hepatic ischemia-reperfusion cells,to explore the protective effects on hepatic ischemia-reperfusion cells.