中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (33): 6124-6126.doi: 10.3969/j.issn.1673-8225.2011.33.011

• 组织构建实验造模 experimental modeling in tissue construction • 上一篇    下一篇

新西兰白兔非乙醇性脂肪性肝病模型的建立与评价

季  榕1，唐  莉2   

  1. 1新疆石河子大学医学院第一附属医院感染科，新疆维吾尔自治区石河子市 832008
    2新疆医科大学第一附属医院感染科，新疆维吾尔自治区乌鲁木齐市 830054
  • 收稿日期:2011-05-13 修回日期:2011-07-07 出版日期:2011-08-13 发布日期:2011-08-13
  • 作者简介:季榕，女，1967年生，汉族， 1991年新疆医科大学毕业，硕士，副主任医师，主要从事肝病研究工作。 jirong@sina.cn

Establishment and evaluation of nonalcoholic fatty liver disease model in New Zealand rabbits

Ji Rong1, Tang Li2   

  1. 1Department of Infectious Disease, First Affiliated Hospital of Medical School of Shihezi University, Shihezi  832008, Xinjiang Uygur Autonomous Region, China
    2Department of Infectious Disease, First Affiliated Hospital of Xinjiang Medical University, Urumqi  830054, Xinjiang Uygur Autonomous Region, China
  • Received:2011-05-13 Revised:2011-07-07 Online:2011-08-13 Published:2011-08-13
  • About author:Ji Rong, Master, Associate chief physician, Department of Infectious Disease, First Affiliated Hospital of Medical School of Shihezi University, Shihezi 832008, Xinjiang Uygur Autonomous Region, China jirong@sina.cnjirong@sina.cn

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233

被引次数

1

摘要：

背景：高脂饮食是导致非乙醇性脂肪性肝病发病的独立相关危险因素。
目的：建立非乙醇性脂肪性肝病兔模型。
方法：将新西兰白兔随机分为对照组和模型组，模型组给予高脂饮食，对照组给予普通动物饲料喂养。
结果与结论：兔饲养12周后，模型组肝细胞均呈现弥漫性脂肪变性，汇管区与小叶间可见炎细胞浸润、坏死及纤维化，对照组肝脏无异常，且模型组肝指数、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、三酰甘油均高于对照组(P < 0.01或P < 0.05)。说明实验成功建立了非乙醇性脂肪性肝病兔模型。

关键词: 脂肪性肝病, 非乙醇性, 新西兰白兔, 动物模型, 组织构建

Abstract:

BACKGROUND: Fat-rich diet is an independent risk factor of nonalcolholic fatty liver disease.
OBJECTIVE: To establish a rabbit model of nonalcolholic fatty liver disease.
METHODS: New Zealand rabbits were randomly divided into a control group and a model group. The model group rabbits were given fat-rich diet and the control group rabbits were given standard diet.
RESULTS AND CONCLUSION: After raise for 12 weeks, hepatocytes of the model group rabbits developed diffuse fatty degeneration, inflammatory cell infiltration, necrosis and fibrosis were observed in the portal area and lobules. Abnormal liver was not observed in the control group. Liver index (liver weight/weight×100%), serum alanine aminotransferase, aspartate aminotransferase, and triacylglycerol levels were significantly higher in the model group than in the control group (P < 0.01 or P < 0.05). These results showed that a rabbit model of nonalcolholic fatty liver disease was successfully established.

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