Carbon tetrachloride (CCl₄) is widely used to establish animal models of liver injury. After free radicals generated from CCl₄ metabolism enter the body, they are activated by cytochrome P450 in the liver to produce trichloromethyl radicals and trichloromethyl peroxyl radicals. These radicals attack phospholipid molecules on liver cell membranes, causing chloroalkylation and lipid peroxidation of cell membranes and endoplasmic reticulum membranes, thus damaging cell membranes and organelles. They can also covalently bind to membrane lipids and protein macromolecules, affecting protein metabolism and disrupting the structural and functional integrity of membranes. Increased calcium ion influx impairs normal cellular physiological functions, ultimately leading to leakage of soluble enzymes from the hepatocyte cytoplasm and cell death.

Balb/c mice (female, 4 weeks old)
Modeling method: Intraperitoneal injection of carbon tetrachloride in olive oil solution twice a week for 12 consecutive weeks. After the last injection of carbon tetrachloride, combined injection of D-galactosamine and lipopolysaccharide was performed to successfully establish an acute-on-chronic liver failure model.
Evaluation indicators: HE staining, Masson staining

HE staining of liver tissue

Masson staining of liver tissue