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【目的】探讨硫化氢（H2 S）对肝纤维化大鼠肝脏缺血再灌注损伤（HIRI）的保护作用。【方法】32只SD大鼠通过胆总管结扎法建立大鼠肝纤维化模型，随机分为4组：①假手术组（Sham组），② HIRI组，③硫化氢钠（NaHS）预处理组（NaHS组），④NaHS预处理＋ PI3K抑制剂组（LY294002组）。检测各组谷草转氨酶（Aspartate transaminase ，AST）、谷丙转氨酶（Alanine aminotransferase ，ALT）、超氧化物歧化酶（Super‐oxide Dismutase ，SOD）、丙二醛（Malondialdehyde ，MDA）水平；取左肝外叶组织，透射电镜观察肝细胞细胞中自噬泡情况；Western Blot技术检测各组细胞自噬相关蛋白Beclin1、LC3B及Akt表达水平。【结果】与Sham组比较，其他三组AST 、ALT、MDA水平均显著升高（ P ＜0．05），其中NaHS组较 HIRI组损伤减轻（ P ＜0．05），LY294002组较NaHS组损伤加重（ P ＜0．05），SOD 改变与之相反。与Sham组比较，其他各组自噬泡均增多，其中NaHS组较HIRI组自噬体减少，LY294002组较NaHS组自噬体增多，自噬相关基因表达发生相应的改变。【结论】外源性H2 S对肝纤维化大鼠HIRI发挥保护作用的机制之一，可能是通过PI3K／Akt信号通路抑制细胞自噬作用来实现的。“,”[Objective] To explore the relationship between the protective effects of hydrogen sulfide on hepatic fibrosis in a rat model of liver ischemia‐reperfusion injury and PI3K/Akt1 pathway .[Methods]A total of 32 Sprague‐Dawley (SD) rats were randomly divided into 4 groups of sham ,hepatic ischemia‐reperfusion in‐jury (HIRI ) , sodium hydrosulfide preconditioning (NaHS ) and NaHS pretreatment + PI3K inhibitor (LY294002) ( n = 8 each) .After reperfusion ,the levels of aspartate transaminase (AST ) ,alanine amin‐otransferase (ALT) ,superoxide dismutase (SOD) and malondialdehyde (MDA) were detected and autophagy vacuoles observed by transmission electron microscope .And the protein levels of Beclin1 ,LC3B and AKt in left hepatic lobe tissue by Western blot .[Results]Compared with sham contrast ,the levels of AST ,ALT and MDA were significantly elevated in three other groups ( P<0 .05) .Injury was less in NaHS group than HIRI group ( P <0 .05) and LY294002 group was more severe than NaHS group ( P<0 .05) .And similar results were obtained in autophagy .[Conclusion] One of the protection mechanisms of exogenous hydrogen sulfide working for hepatic fibrosis may be inhibiting autophagy via PI3K/Akt signaling pathway in rats of liver ische‐mia‐reperfusion injury .