摘要肝性脑病(Hepatic encephalopathy，HE)是终末期肝病的主要并发症，可造成认知障碍、注意力减退和运动功能障碍，重者昏迷、死亡。HE发病机制复杂，高氨血症对星形胶质细胞的毒性作用如神经递质的改变、氧化应激、星形胶质细胞肿胀，被认为是HE发病的核心因素。此外，大量证据表明神经炎症也参与了HE的发生发展，但具体机制尚未完全阐明。文章总结了HE中神经炎症的形成、表现及可能参与的诱发因素，并阐述了其通过改变神经递质的膜表达和脑代谢影响运动功能和认知，且这些改变是可逆转的。

abstractsHepatic encephalopathy(HE) is a major complication in patients with end-stage liver disease and it can cause cognitive impairment, attention loss, and motor dysfunction, even coma or death. The pathogenesis of hepatic encephalopathy is complex. Hyperammonemia is considered to be the central pathogenesis because its toxic to astrocytes such as changes of neurotransmitters, oxidative stress, and astrocyte swelling. In addition, lots of evidence indicate that neuroinflammation is involved in the development of HE. However, the specific mechanism has not been fully elucidated. This review summarizes the production, performance and the mechanism of neuroinflammation in HE and it clarifies neuroinflammation impairs motor function and cognitive by changing the membrane expression of neurotransmitters and metabolism changes in brain, and these alterations are reversible.