动物模型,胆囊炎 z-bo 2020-08-07 619

　　(1) Reproduction method Guinea pigs, male or female, weighing 300-400g, intraperitoneally injecting Lincomycin hydrochloride (LIN) at a dose of 60mg/kg body weight, 1 time/d for 7 consecutive days; or 300mg/kg body weight Lithocholic acid (LCA) was administered at a dose, once a day, for 15 consecutive days; or a one-time intramuscular injection of a-naphthylisothiocyanate (ANIT) at a dose of 200 mg/kg body weight. 7 to 35 days after administration, blood was collected to prepare serum, the gallbladder was removed by laparotomy, bile was extracted after weighing, and the bile was collected for biochemical analysis, and the contents of the gallbladder were observed by naked eyes and microscope. The gallbladder tissue was organized by light microscope and enzyme histochemical techniques. Morphological and enzymatic histochemical examination.

　　(2) Model characteristics Lincomycin and lithocholic acid can both reduce animal weight, increase the volume of the gallbladder, and increase the number of stones in the cyst. Among them, in the lincomycin model in its early stage (experiment 7d), most animals were accompanied by hypersecretion of mucosal glands, submucosal and lamina propria edema and a large amount of exuding fibers. In the later period (experiment 14-35d), gallbladder lesions were chronic Proliferative inflammation, manifested by obvious proliferation of epithelial cells, increased mucosal folds and recessed crypts in the lamina propria, and deep mucosal depression

　　Layer formation of Rokitansky-Aschaff; Lithocholic acid model shows liver cell degeneration and necrosis, liver cell function decline, bile metabolism disorder, and endogenous β-glucuronidase (β-GCD) activity increases , Ca2+, etc. increase; the sulfhydryl acid-a-naphthyl ester model presents acute proliferation of mucosal epithelial cells, general increase in goblet cells, rich mucosal folds and submucosal crypts, proliferation of lamina propria glands, and most of them are double ductal vesicles The glands are formed by Luo-Adu.

　　(3) Comparative medicine The etiology of human cholecystitis is not only closely related to gallstones, but also related to factors such as changes in bile components, cholestasis, infection and immune function, and antibiotic allergy. Ordinary guinea pigs are allergic to antibiotics, and their normal intestinal flora can easily produce endotoxin when combined with antibiotics. The latter can cause cholecystitis in guinea pigs. Lincomycin, as an antibiotic, can cause a guinea pig cholecystitis model characterized by jaundice and elevated transaminases and accompanied by stones. The biggest disadvantage of this model is the high mortality rate. Lithocholic acid is one of the metabolites of cholesterol in the body. Excessive lithocholic acid can cause damage to the liver and cause cholesterol and bile acid metabolism disorders. A large number of repeated administrations of lithocholic acid can cause changes in the total bilirubin, conjugated bilirubin, total cholesterol and other components in the bile of guinea pigs, triggering massive proliferation of bile duct cells and fibers, leading to chronic proliferative cholecystitis. The sulfhydryl acid-a-naphthyl ester cholecystitis model belongs to the cholestatic type, which manifests as acute proliferative cholecystitis.