间歇性低氧对小鼠非酒精性脂肪肝形成影响-病理学与病理生理学专业论文.docxVIP

Ab Abstract Ab Abstract PAGE PAGE IV PAGE PAGE V ABSTRACT Objective: To study and observe the influence of intermittent hypoxia on the formation of nonalcoholic fatty liver disease in mice and its mechanism, for exploring new ways and means of clinical prevention and treatment of nonalcoholic fatty liver disease. Method: The model of non-alcoholic fatty liver disease was established by feeding with high fat and sugar in mice; The role of the low oxygen (15%)environmental stimuli and its work time were determined by the AMPK activity in liver cells; Lesion degree was determined by conventional pathological methods and the effects of intermittent hypoxia and metformin on the pathological process of nonalcoholic fatty liver disease in mice. The experimental groups and steps: Establish the model of non-alcoholic fatty liver disease in mice: A closed group of 30 Kunming(Km) male mice were randomly divided into normal control group and high fat and sugar model group. And then, the changes of weight were measured and the degrees of liver fat were observed until the model of non-alcoholic fatty liver disease was established. Screen the working time of 15% low oxygen environmental stimulus: 25 Km male mice were randomly divided into 5 groups: groups treated with low oxygen for1h, 2 h and 4 h, and normal control group and group treated with metformin.They were given ordinary feed. At the end of the experiment, the mice were anesthetized and executed, and then the livers were collected. The AMPKa activity was detected by Western blotting to screen the working time of 15% low oxygen environmental stimulus. (3)The effects of intermittent hypoxia on the pathological process of nonalcoholic fatty liver disease in mice: 48 Km male mice were randomly divided into 4 groups: group A blank control group, group B high fat and sugar model group, group C low oxygen intervention group, and group D Metformin group. The changes of the weight were weighed and recorded once a week. Group