【Animal Modeling】-Acute rabbit atherosclerotic plaque animal model caused by the combination of high cholesterol feeding method and immune method

  (1) Breeding method Place adult male rabbits in a separate cage for observation for 1 week, record fasting weight, collect blood to measure various blood lipid indexes, and then inject bovine serum albumin intravenously once. 250 mg/kg body weight) start taking it immediately. Fat feed, the formula is: 30% cholesterol, 10% lard, 2% sodium deoxycholate, 2% propylthiouracil. After compulsory oral intake of a high-fat diet with a body weight of 2 ml/kg every day, supplement the regular diet and drink freely for a total of 6 weeks of feeding. After 3 weeks of high-fat diet, the serum TC and LDL of the model rabbits increased significantly, about 26.8 times and 58.3 times, respectively. There are obvious yellow atherosclerotic plaques of various sizes on the arterial wall. The arterial intima shows discontinuous mounds. Or the new moon is bulging, and a large number of lipid-containing foam cells will proliferate under the inner membrane, causing single cells to swell, collapse and liquefy. Others were given rabbit serum albumin 5 mg/kg intravenously every other day and received a 0.5% high-cholesterol diet for 10 consecutive weeks. Serum TC and TG levels were significantly increased, and lipid plaques were found in the aortic intima. Plaques, infiltration of a large number of macrophages and T lymphocytes, smooth muscle cell migration and proliferation, but no fibrous caps.

  (2) This model is characterized by a single injection of bovine serum albumin (250 mg/kg body weight) on a high-fat diet. It takes a short time to create the model. The pathological changes are typical, reliable and practical. The high-fat feed formula used contains sodium deoxycholate, which can promote the digestion and absorption of lipids, and propylthiouracil can inhibit the synthesis of thyroxine, thereby reducing the metabolism and lipid consumption of rabbits. Compared with today's commonly used high-fat feed formula (only containing cholesterol and fat), this formula can increase blood lipid content. Compared with the latter (conventional feeding) method, high-fat tube feeding is more reliable and has complete absorption capacity, but it is not as simple as the latter. Importing exogenous protein (serum albumin) at the same time can reduce modeling time. This is a fast, stable and effective As model.

  (3) Comparative medicine. Hyperlipidemia is closely related to the occurrence of As. Elevated serum TC levels will accelerate the progression of As and its cardiovascular diseases. Elevated LDL and TG are also risk factors for the development of As. This model is fed a high-fat diet, which can cause hyperlipidemia and atherosclerotic plaques in rabbits. This is consistent with the eating habits and clinical symptoms of patients with clinical hyperlipidemia and atherosclerotic plaque. Three weeks after the former model, the serum biochemical indicators of the model animal indicated that the model was in the early stage of As. After six weeks, obvious atherosclerotic plaque appeared on the arterial wall, which was in line with typical clinical symptoms. As. The latter modeling method showed macrophages, T lymphocyte infiltration, smooth muscle cell migration and proliferation after 10 weeks, but no fibrous caps were observed. This is the early stage of As disease, and the modeling time is very long.