肝衰竭病死率高，严重威胁患者的健康。因此探寻有效的治疗新靶位和新方法来降低病死率十分关键。本团队发现AMSC-Exo尾静脉输注LPS/D-GalN诱导的肝衰竭小鼠后，其可抵达肝脏巨噬细胞，并减少肝脏炎性细胞浸润和炎症因子分泌，死亡率显著降低。进一步分析发现AMSC-Exo中高表达miR-17，而它与控制细胞凋亡，招募、炎性因子分泌相关的ASK1存在靶向调控关系。因此本项目拟通过研究了解，在肝衰竭进程中ASK1表达是否与不同来源的肝脏巨噬细胞的功能调控有关；AMSC-Exo中miR-17是否可通过靶向抑制ASK1影响Kupffer的凋亡，炎性、招募因子分泌，是否可影响MoMs的形成和功能塑造。最终明确AMSC-Exo中miR-17在肝衰竭治疗中的作用，以及通过分析它在不同来源肝脏巨噬细胞中分别起到的作用探索肝衰竭治疗的最佳时间窗口，为今后临床应用AMSC-Exo输注治疗肝衰竭提供理论依据。

The liver failure causes high rate of death seriously threatens health of the patients. So it is crucial to find new targets and methods to reduce mortality. Our team found that by injecting the AMSC-Exo in the LPS/D-GalN induced liver failure mice via tail vein, both of the macrophage infiltration and inflammatory factor secretion decreased, resulting in less mortality rate. Further analysis shows that the miR-17 was high expression in the AMSC-Exo, which could inhibit post transcriptional regulation of gene ASK1, resulting less cells apoptosis, recruitment factor and inflammatory factor secretion. So this project is intended to study the relationship between the ASK1 and the function regulation of different source of macrophage; and to understand whether the miR-17 in AMSC-Exo could affect the kupffer cells apoptosis, recruitment factor and inflammatory factor secretion by inhibition the expression of ASK1; or whether the miR-17 could affect the formation and function molding of peripheral mononuclear macrophage. Finally to clear that the key role of miR-17 in treatment of liver failure with AMSC-Exo, and to find the best time windows for injection the AMSC-Exo, which could provide basis for future clinical application.