Objective To Investigate the pathogenetic mechanism of nonalcoholic fatty liver disease (NAFLD) in gerbils, the changes in the lipid metabolism, liver function and antioxidation in its development caused by high fat diet.Methods One hundred and twenty gerbils were divided randomly into 2 groups: the model group fed with high fat diet and control group fed with normal diet. Ten gerbils were killed at 1, 2, 4, 6, 8 and 16 weeks after the start of diet,respectively. The pathological changes of the liver were examined, and the liver index, serum CHO, TG, LDL-c, HDL-c,GOP, GPT, the liver SOD, GSH-PX, CAT, FFA were determined. Results In the model group, simple fatty liver was observed at 2 weeks, mild inflammation in the hepatic portal areas at 6 weeks, focal perisinosodal fibrosis/pericellular fibrosis of acini band at 8 weeks, and moderate liver fibrosis at 16 weeks after the start of diet. CHO,HDL-C,LDL-C and FAA were obviously elevated (P ＜ 0. 05 ,P ＜ 0. 01 )at 1,2,4,6,8,16 weeks, TG was raised at 1,2,4 weeks( P ＜ 0. 05,P ＜ 0. 01 ), GOT and GPT were Sisnificantly increased after 16 weeks(P ＜ 0. 01 ), GSH-PX、 CAT and SOD were Significantly decreased after 8 weeks ( P ＜ 0.05, P ＜ 0. 01 ). Conclusions Gerbil models of simple fatty liver can be developed at 2 weeks after high fat diet feeding, and moderate liver fibrosis after 16 weeks. Lipid metabolic disorders and oxidative stress play different roles in the development of nonalcoholic fatty liver disease.%目的 分析高脂饮食导致的沙鼠NAFLD疾病进展中脂质代谢、肝功能、抗氧化等方面的变化,探讨沙鼠NAFLD的形成机理.方法 雄性沙鼠120只,随机分为对照组和模型组.对照组给予普通饲料,模型组高脂饮食建立NAFLD模型.分别于1、2、4、6、8、16周每组各处死10只动物,观察肝脏病理变化,计算肝指数,检测血清CHO、TG、LDL-C、HDL-C、GOP、GPT及肝组织的SOD、GSH-PX、CAT活性和FFA含量.结果 模型组病理观察2周形成单纯性脂肪肝,6周动物门管区有轻度炎症,8周出现腺泡Ⅲ带局灶性窦周/细胞周纤维化,16周肝脏中度纤维化;模型组第1、2、4、6、8、16周时CHO、HDL-C、LDL-C及FAA波动性升高,但均高于同期对照组(P<0.05,P<0.01),TG在1、2、4周高于同期对照组(P<0.05,P<0.01);16周末GOT、GPT出现了显著性升高(P<0.01).抗氧化酶GSH-PX、CAT、SOD活性模型组在第8～16周显著性降低(P<0.05,P<0.01).结论 高脂饮食使沙鼠2周形成单纯性脂肪肝模型后,随饲喂时间延长,16周末可发展为中度肝纤维化.脂质代谢紊乱与氧化应激在沙鼠NAFLD进展中的发挥了不同的作用.
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