对乙酰氨基酚(acetaminophen,APAP)毒性是发达国家药物引起的急性肝衰竭的主要原因。大量肝细胞坏死是APAP肝毒性的主要特征,损伤肝细胞的再生是至关重要的,许多因素会影响肝脏修复。炎症在APAP过量导致肝损伤后再生中起着重要作用,但其机制仍不清楚。目前,通常认为炎症是引起肝组织损伤的主要原因,然而证据表明炎症在早期阶段导致肝损伤,但在后期阶段可以促进肝脏再生。核因子-κB(nuclear factor kappa B,NF-κB)是APAP肝损害的一个重要炎性调节因子,然而NF-κB活性增加与肝损伤后期阶段的肝脏再生有密切关系。肿瘤坏死因子-α作为一种早期炎性细胞因子,也同APAP肝损伤后肝脏再生相关。炎症在APAP肝损伤中起着双重作用,即参与了早期肝损伤过程又参与了后期的肝脏再生过程。 Acetaminophen (APAP) toxicity is the leading cause of acute drug-induced liver failure in developed countries. Massive hepatocyte necrosis is a major feature of APAP hepatotoxicity, which is crucial to impair the regeneration of hepatocytes, and many factors can affect liver repair. Inflammation plays an important role in the regeneration of APAP-induced liver injury, but the mechanism remains unclear. Currently, inflammation is generally considered the leading cause of liver tissue damage, however evidence suggests that inflammation leads to liver damage at an early stage but promotes liver regeneration at a later stage. Nuclear factor kappa B (NF-κB) is an important inflammatory regulator of APAP hepatic injury. However, the increase of NF-κB activity is closely related to liver regeneration in the late phase of liver injury. Tumor necrosis factor-alpha, an early inflammatory cytokine, is also associated with hepatic regeneration following APAP liver injury. Inflammation plays a dual role in APAP liver injury, which is involved in the process of early liver injury and later in the liver regeneration process.