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目的:探讨间歇性低氧对小鼠非酒精性脂肪肝(NAFLD)形成的影响。方法:采用高脂高糖饮食诱发小鼠NAFLD;Western blot检测肝细胞磷酸化腺苷酸激活的蛋白激酶(p-AMPK)的表达水平并确定起效时间;常规病理学观察肝脏病变程度,血液生化测定肝功能、血糖和血脂水平,比较观察间歇性低氧与二甲双胍对小鼠NFALD病理学进程的影响。结果:高脂高糖饮食诱导4周成功复制小鼠可逆性NFALD模型;置15%低氧环境1 h即可激活肝细胞AMPK活性;与正常组比较,模型组有严重肝
Objective: To investigate the effect of intermittent hypoxia on the formation of non-alcoholic fatty liver disease (NAFLD) in mice. Methods: NAFLD was induced in mice with high-fat and high-sugar diet. Western blot was used to detect the expression of phosphorylated adenylate-activated protein kinase (p-AMPK) in hepatocytes and the onset time. The pathological changes of hepatic lesions, Biochemical determination of liver function, blood glucose and lipid levels, compared intermittent hypoxia and metformin on NFALD pathological process in mice. RESULTS: The reversible NFALD model of mice successfully replicated in high-fat and high-sugar diet for 4 weeks and AMPK activity in hepatocytes activated by 15% hypoxia for 1 h. Compared with the normal group, the model group had severe liver