Inflammation plays a dual role in acetaminophen hepatotoxicity
Runkuan YANG
Abstract：Acetaminophen (APAP) toxicity is the leading cause of drug-induced acute liver failure in the developed countries. Massive hepatocyte necrosis is the predominant feature of APAP hepatotoxicity, therefore, the liver regeneration is vital for survival after the toxic insult and many factors can influence liver repair. Inflammation can significantly influence hepatic regeneration after APAP overdose and the role of inflammation in APAP induced acute fatal liver injury is still not clear. Currently, inflammation is still frequently considered to be responsible for liver tissue damage, however, emerging evidence shows that inflammation contributes to liver injury at early phase but improves hepatic regeneration during the late phase of APAP hepatotoxicity;nuclear factor kappa B is an important regulator of inflammation, however, enhanced nuclear factor kappa B activation is associated with improved liver recovery at the late phase of APAP overdose;tumor necrosis factor-αis a typical early inflammatory cytokine, however, increased tumor necrosis factor-αconcentration is associated with improved hepatic regeneration at the late phase of APAP toxicity. These results indi-cate that inflammation plays a dual role in APAP overdose: inflammation contributes to liver injury at early phase but improves hepatic regeneration at the late phase of APAP induced acute liver injury.
Keywords：AcetaminophenHepatotoxicityInflammationRegenerationNuclear factor kappa B (NF-κB)
Publication Date：2016-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 129-133 )