Objective To prepare a stable rat model of chronic liver failure and provide a method for basic research. Methods 66 SPF SD rats were divided into normal group (18 rats) and modeling group (48 rats). The modeling group was intraperitoneally injected with 50% CCl4 olive oil solution (1.5 ml/kg, twice a week), and multidimensional assessment was performed at 8, 16 and 24 weeks, respectively. The evaluation included: ultrasonic examination of liver morphology, hardness, portal vein diameter and ascites; Serum, plasma and liver tissue were collected to detect liver function (AST, ALT, TBIL), coagulation function (PT, INR) and blood ammonia level. The degree of liver tissue injury and fibrosis was observed by HE staining and Masson staining. Water maze test to assess cognitive function; The survival rate and pathological changes of gross hepatic tissue were recorded simultaneously. Results Compared with the normal group, the rats in the model group showed decreased activity, decreased appetite, yellow urine and increased abdominal circumference. Ultrasound showed that the liver parenchymal echo of the model group was enhanced and thickened with time, secondary ascites formation, portal vein dilation and portal hypertension. At 24 weeks, water maze and blood ammonia tests confirmed cognitive decline (memory and orientation loss) and hepatic encephalopathy in the model group. The gross observation showed that the liver in the model group was rough and uneven in appearance and atrophied in volume. Histologically, HE staining showed hepatocyte swelling, steatosis and necrosis. Masson staining confirmed fibrosis progression with pseudolobule formation. 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. Conclusion The rat model constructed by intrabitoneal injection of 50% CCl4 olive oil solution (1.5 ml/kg/ week) for 24 weeks can stably simulate persistent chronic liver injury, and lead to the typical pathological changes and complications of chronic liver failure based on the decompensation stage of cirrhosis. The model completely replicates the pathological evolution chain of human hepatitis → liver fibrosis → liver cirrhosis compensation → decompensation → chronic liver failure, providing a reliable modeling reference for the study of chronic liver failure mechanism.