动物造模,肝纤维化 z-bo 2022-02-02 506

　　(1) Replication method Adult male rats were intraperitoneally injected with thioacetamide (TAA) at a dose of 100 mg/kg body weight. The first dose was doubled, and then intraperitoneally injected once every other day for 13 consecutive weeks. Or mix TAA into a 30% solution with physiological saline as the only drinking water for the animal, and feed it continuously for 17 weeks. After modeling, take whole blood and extract liver tissue for biochemical and histomorphological examination.

　　(2) Model features: Injecting TAA 100mg/kg body weight for 13 consecutive weeks, the model animals have decreased activity, reduced food intake, slow response to sound and light, and increased plasma alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activities , Plasma endotoxin (PLS) and liver tissue hydroxyproline (HYP) levels increase, the fibrils in the portal area of the liver tissue proliferate and extend into the lobules, and part of the fibers separate the liver lobules, accompanied by degeneration, necrosis, and liver cell Cell regeneration, inflammatory cell infiltration in the portal area. Continuously drinking 30% TAA water solution, liver fibrosis occurred at 8 weeks, and liver cirrhosis occurred at 17 weeks.

　　(3) Comparative medicine TAA is a weak carcinogen, which can cause hepatocyte necrosis and liver fibrosis, even cirrhosis and tumors. After TAA enters the body, it prolongs the mitotic process of hepatocytes and hinders the transfer of RNA from the nucleus to the cytoplasm, which in turn affects the enzyme-dependent metabolic process, and ultimately leads to hepatocyte necrosis. The destruction of liver parenchyma leads to increased production of connective tissue in the interstitium , Thereby causing the local deposition of fibrous tissue. In addition, TAA not only damages the liver parenchymal cells, but also damages the intestinal mucosal barrier function. The endotoxin in the intestine is absorbed by the portal vein in large quantities. At the same time, due to the severe dysfunction of the liver macrophages (Kupffer) cells, it enters the liver. Toxins cannot be processed and eliminated, and flow into the systemic circulation to form intestinal endotoxemia, which further deteriorates liver function. According to the characteristics of the formation of this model, it can be used to study the mechanism of liver fibrosis during the transformation of chronic liver disease into cirrhosis and liver cancer.