Ethanol is closely related to the occurrence of liver fibrosis. After ethanol is absorbed in the gastrointestinal tract, it is oxidized by the enzyme system of the body to acetaldehyde and can be further oxidized to acetate. During the process of ethanol converting to acetaldehyde and acetaldehyde converting to acetate or acetyl coenzyme iA (NAD), reducing nicotinamide adenine dinucleotide (NADH) can also be produced. The decrease in the NAD/NADH1 ratio inhibits the trihydroxy acid cycle in the liver, weakens gluconeogenesis, and increases lipid acid synthesis. When the increase exceeds the liver's processing capacity, fatty liver is formed, and eventually liver fibrosis occurs. According to the causes and onset of human alcoholic liver disease! The mechanism was replicated by continuously injecting ethanol into the stomachs of rats while feeding them solid feed for 24 weeks. Rat models for observing changes in general behavioral activities, serum biochemical indicators and histomorphology of animals during the same period. The main feature of this model is that it can observe and evaluate the pathological changes of chronic alcoholic liver disease at each stage except for alcoholic cirrhosis induced by single-factor ethanol through biochemical and morphological indicators. It is relatively in line with the clinical reality of humans. Moreover, it has a high fibrosis and film formation rate, stable model, relatively short modeling cycle, convenient operation and low cost. It has been widely used in China.

At 4 weeks after modeling, the animals showed phenomena such as runnose, dull posture, drowsiness, listlessness, loss of appetite and slow movement. The contents of serum aspartate aminotransferase (AST) and alkaline phosphatase (ALP) increased, while the contents of total albumin (TP) and globule albumin (GP) decreased. Bridging necrosis occurred in the central area - portal area of adjacent hepatic lobules in the liver tissues of some rats. A large number of inflammatory cell infiltrations can be seen in the necrotic area, mainly neutrophils, presenting with moderate to severe inflammatory changes. At 12 weeks, the luster of the animal hair decreases, the weight gain is slow, loose stools are frequent, the liver volume becomes larger, the color is dull, and the texture is relatively hard. The liver tissues of most animals show varying degrees of hydrodegeneration and balloon degeneration, which are obvious in the hepatocytes under the liver capsule, and the steatosis of hepatocytes is aggravated, with an increase in lipid droplets. At 24 weeks, the serum AST of the animals remained at a relatively high level, the ALP recovered from a high level to the normal range, the albumin (ALB) content decreased significantly, and blood stasis could be seen in the small arteries and veins of the hilar area, the central vein of the hepatic lobule, and the hepatic sinusoids. Clear blood appeared in the central vein, some central veins were dilated, and the basement membrane was thickened. The vascular endothelial cells and sinus endothelial cells are swollen, and collagen fibers deposit along the sinus wall, presenting a barbed wire grid or turtle shell-like appearance. The coverage is relatively wide, and they can also be seen in the portal area and its surrounding areas. In severe cases, the collagen fibers in the central vein and portal area thicken, and fibrous septa appear in the lobules.