Wilson病（WD）肝纤维化是铜离子在肝脏沉积引起慢性损伤后的一种修复反应，最终导致肝硬化，甚至引起患者死亡，早期干预是治疗的重要手段。我们前期研究已证实肝豆扶木汤（GDFMT）对WD具有良好疗效，并发现WD肝纤维化模型TX小鼠肝组织中差异性表达基因——miRNA-29，GDFMT可上调其表达。研究表明，自噬在肝纤维化的发生发展中起重要作用，它能为启动和维持肝星状细胞（HSC）活化提供必需能量。miRNA-29的靶基因ULK1参与调控细胞自噬的起始阶段。因此我们提出假说：“GDFMT可通过上调miRNA-29调控靶基因ULK1介导的细胞自噬，抑制HSC活化从而治疗WD肝纤维化”。本研究以TX小鼠和原代HSC为模型，采用体内、体外实验相结合方式，从“miRNA-29→ULK1→自噬”三个环节探讨GDFMT治疗WD肝纤维化分子机制，对深化其发病机制和中医药效应研究具有重要的理论与现实意义。

Wilson's disease liver fibrosis is a kind of repairing reaction after chronic damage caused by copper ion deposition in the liver, which eventually leads to cirrhosis and even the death of patients. Early intervention is an important strategy for treating Wilson's disease liver fibrosis. Our previous studies have confirmed that GDFMT has a good anti-fibrosis effect. miR-29 is significantly decreased in TX mice, which can be upregulated by GDFMT. Studies have shown that autophagy plays an important role in the development of liver fibrosis, which provides the necessary energy to initiate and maintain the activation of hepatic stellate cells (HSC).The target gene of miRNA-29, ULK1, is involved in the regulation of the initial stage of autophagy. Therefore, we hypothesized that "GDFMT can extenuate WD liver fibrosis by up-regulating miRNA-29 targeting ULK1 to regulate autophagy and inhibiting HSC activation." TX mice and primary HSC were used as models to study the molecular mechanism of GDFMT in the treatment of WD liver fibrosis from the three links of "miRNA-29→ULK1→autophagy" in vivo and in vitro experiments. This study has important theoretical and practical significance for deepening pathogenesis and research on the effect of Chinese medicine.