Objective To prepare a stable rat model of chronic liver failure to provide a tool for basic research. Methods Sixty-six SPF SD rats were divided into a normal group (n= 18) and a modeling group (n=48). Rats in the modeling group received an intraperitoneal injection of 50% CCl₄ olive oil solution (1.5 mL/kg, twice a week). Multidimensional assessment was performed at 8, 16, and 24 weeks, respectively, including ultrasonic examination of liver morphology, hardness, portal vein diameter, and ascites, and collection of serum, plasma, and liver tissue to detect liver function, coagulation function, and blood ammonia levels. Liver tissue injury and fibrosis were observed by hematoxylin-eosin(HE) and Masson staining. Cognitive function was assessed using the water maze test. Survival were recorded simultaneously. Results Rats in the model group showed decreased activity and appetite, yellow urine, and increased abdominal circumference compared with the normal group. Ultrasound showed enhanced liver parenchyma echo in the model group that thickened with time, secondary ascites formation, portal vein dilation, and portal hypertension. Water maze and blood ammonia tests confirmed cognitive decline (memory and orientation loss) and hepatic encephalopathy in the model group. Gross observation showed that the liver in the model group was atrophied and appeared rough and uneven. HE staining showed hepatocyte swelling, steatosis, and necrosis, and Masson staining confirmed fibrosis progression with pseudolobule formation. The liver function indexes AST, ALT, TBIL and blood ammonia continued to increase, and coagulation dysfunction (prolonged PT and increased INR) gradually increased with the modeling process. Conclusions Intraperitoneal injection of 50% CCl₄ olive oil solution (1.5 mL/kg,every week) for 24 weeks can stably simulate persistent chronic liver injury in rats and lead to the typical pathological changes and complications of chronic liver failure, based on the decompensation stage of cirrhosis. This model replicates the pathological evolution of human hepatitis from liver fibrosis → liver cirrhosis compensation → decompensation → chronic liver failure, providing a reliable modeling reference for the study of the mechanism of chronic liver failure.