Acetaminophen, also known as paracetamol, is a commonly used antipyretic and analgesic drug. Low doses do not cause liver injury, while high-dose administration can lead to varying degrees of liver damage. After saturation of conjugation with glucuronic acid or sulfuric acid, the remaining acetaminophen is metabolized by cytochrome P450 to produce excessive N‑acetyl‑p‑benzoquinone imine (NAPQI). NAPQI can be detoxified by binding to glutathione; however, when glutathione is insufficient, excess NAPQI forms covalent bonds with proteins in hepatocytes, resulting in hepatocellular injury. Animal models of acetaminophen-induced liver injury are widely used for screening therapeutic agents against hepatocyte injury caused by reduced glutathione levels due to various causes. As a classic drug-induced liver injury model, the main morphological feature is massive centrilobular necrosis around the central vein, without obvious hemorrhage or steatosis. This model is highly sensitive in mice but not in rats.

C57BL/6 mice (male, 6–8 weeks old)

Modeling method: The liver injury model was established by intragastric administration of acetaminophen for two consecutive weeks.

Evaluation indicators: HE staining, Masson staining

HE staining of liver tissue

Masson staining of liver tissue