Hepatic encephalopathy (HE) is a neurological disorder that occurs in patients with liver insufficiency. However, its pathogenesis has not been fully elucidated. Pharmacotherapy is the main therapeutic option for HE. It targets the pathogenesis of HE by reducing ammonia levels, improving neurotransmitter signal transduction, and modulating intestinal microbiota. Compared to healthy individuals, the intestinal microbiota of patients with liver disease is significantly different and is associated with the occurrence of HE. Moreover, intestinal microbiota is closely associated with multiple links in the pathogenesis of HE, including the theory of ammonia intoxication, bile acid circulation, GABA-ergic tone hypothesis, and neuroinflammation, which contribute to cognitive and motor disorders in patients. Restoring the homeostasis of intestinal bacteria or providing specific probiotics has significant effects on neurological disorders in HE. Therefore, this review aims at elucidating the potential microbial mechanisms and metabolic effects in the progression of HE through the gut–brain axis and its potential role as a therapeutic target in HE.

肝性脑病（HE）是一种发生于肝功能不全患者的神经系统疾病。然而，其发病机制尚未完全阐明。药物治疗是 HE 的主要治疗选择。它通过降低氨水平、改善神经递质信号转导和调节肠道微生物群来针对 HE 的发病机制。与健康个体相比，肝病患者的肠道菌群存在显着差异，且与HE的发生相关。此外，肠道菌群与HE发病机制的多个环节密切相关，包括氨中毒理论、胆汁酸循环、GABA能张力假说、神经炎症等，导致患者认知和运动障碍。恢复肠道细菌的稳态或提供特定的益生菌对 HE 的神经系统疾病具有显着效果。因此，本综述旨在阐明 HE 通过肠-脑轴进展的潜在微生物机制和代谢效应，及其作为 HE 治疗靶点的潜在作用。