脓毒症是宿主对感染反应失调引起的危及生命的器官功能障碍，是临床上常见的危重症。尽管对脓毒症的发病机制有了深入理解，但国内外临床治疗中脓毒症的病死率仍未见明显改善。近年来，自噬在脓毒症发病中的作用成为新的医学研究热点。自噬在脓毒症中可能通过清除病原微生物、中和微生物毒素、调节细胞因子释放等机制对机体起到保护作用，并在脓毒症时心、肺等器官功能障碍及炎症免疫反应中发挥作用。硫化氢（Hn 2S）可通过多个信号通路激活自噬而发挥作用，如磷酸腺苷依赖性蛋白激酶/哺乳动物雷帕霉素靶蛋白（AMPK/mTOR）、磷脂酰肌醇-3-激酶/丝氨酸苏氨酸蛋白激酶/mTOR（PI3K/Akt/mTOR）、肝激酶B1/STE20相关衔接蛋白/小鼠蛋白25（LKB1/STRAD/MO25）和微小RNA-30c（miR-30c）等。本文就Hn 2S通过影响自噬相关基因酵母ATG6同源物（Beclin-1）、微管相关蛋白1轻链3（LC3）的表达对脓毒症肠功能的影响进行综述，以探讨Hn 2S介导自噬相关基因表达在脓毒症肠功能损伤中的保护作用，为脓毒症治疗提供新的策略。n “,”Sepsis is an organ dysfunction that endangers a patient's life caused by an imbalanced infection response, and is a clinically critical illness. Despite a deep understanding of the pathogenesis of sepsis, there has been no significant improvement in sepsis mortality during clinical treatment at home and abroad. In recent years, the role of autophagy in the pathogenesis of sepsis has become a new research point in the field of medical research. Autophagy may protect the body by removing pathogenic microorganisms, neutralizing microbial toxins, and regulating cytokine release in sepsis. Studies have shown that autophagy plays a role in heart and lung organ dysfunction and inflammatory immune response in sepsis. Studies have also shown that hydrogen sulphide (Hn 2S) can activate autophagy through multiple signaling pathways, such as adenylate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR), phosphoinositide 3 kinase/Akt/mTOR (PI3K/Akt/mTOR), liver kinase B1/STE20 related adapter protein/mouse protein 25 (LKB1/STRAD/MO25) and microRNA-30c (miR-30c), etc. signaling pathways. This article reviewed the effects of Hn 2S on autophagy-related genes Beclin-1 and microtubule-associated protein light 3 chain (LC3) on intestinal function of sepsis in order to explore the Hn 2S-mediated autophagy gene expression in pus. The protective role of autophagy gene for intestinal dysfunction provides a new strategy for the treatment of sepsis in the future.n