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高脂及MCD饮食诱导非酒精性脂肪性肝炎动物模型的比较
引用本文:续畅,刘泽洲,许可嘉,李健,杨美娟,牛建昭,唐炳华.高脂及MCD饮食诱导非酒精性脂肪性肝炎动物模型的比较[J].生物磁学,2014(18):3451-3455.
作者姓名:续畅  刘泽洲  许可嘉  李健  杨美娟  牛建昭  唐炳华
作者单位:北京中医药大学基础医学院,北京100029
基金项目:国家自然科学基金面上项目(81273884); 高等学校学科创新引智计划资助项目(B07007)
摘    要:目的:对高脂饮食诱发的大鼠NASH模型与蛋氨酸胆碱缺乏饮食诱发的小鼠NASH模型进行血清学及病理学比较,并初步探讨两种模型的发病过程及机制。方法:高脂饮食喂养SD大鼠8周,蛋氨酸胆碱缺乏饮食喂养C57BL/6小鼠2周,以制备NASH模型。取材后,血清用比色法对TG、CHO、FPG的含量进行检测,用放免法对FINS的含量进行检测,并对HOMA-IR指数进行计算;肝组织制成石蜡切片及冰冻切片进行HE及油红O染色,并根据"NAFLD活动度积分"对各组肝组织进行NASH分级评估。结果:高脂饮食大鼠血清中TG、CHO、FPG、FINS的含量显著升高,经计算HOMA-IR指数显著升高;MCD小鼠血清中TG、CHO的含量显著下降,FPG、FINS的含量未发生显著性改变,经计算HOMA-IR指数未发生显著性改变。HE染色、油红O染色及NAFLD活动度积分结果显示,高脂饮食大鼠及MCD小鼠的肝组织均已发展到NASH阶段。结论:两种造模方法均可稳定的模拟人类NASH疾病的血清学及病理学变化,其中高脂饮食诱发的大鼠NASH模型可模拟人类的发病过程及机制,能够复制胰岛素抵抗、氧化应激等人类全身代谢紊乱表现,在NASH研究领域更占优势。

关 键 词:非酒精性脂肪性肝炎  动物模型  比较  病理学  血清学

Comparison of High-fat Diet and Methionine-choline Deficient diet induced by non-alcoholic Steatohepatitis Animal Model
XU Chang,LIU Ze-zhou,XU Ke-jia,LI Jian,YANG Mei-juan,NIU Jian-zhao,TANG Bing-hua.Comparison of High-fat Diet and Methionine-choline Deficient diet induced by non-alcoholic Steatohepatitis Animal Model[J].Biomagnetism,2014(18):3451-3455.
Authors:XU Chang  LIU Ze-zhou  XU Ke-jia  LI Jian  YANG Mei-juan  NIU Jian-zhao  TANG Bing-hua
Institution:(Basic Medical College of Beijing University of Chinese Medicine, Beijing, 100029, China)
Abstract:Objective: Comparison of high-fat diet and methionine-choline deficient diet induced by non-alcoholic steatohepatitis animal model in serology and pathology, and explore the pathogenesis and mechanism. Methods: SD rats feed high-fat diet and C57BL/6 mice feed methionine-choline deficient diet to become model of non-alcoholic steatohepatitis. Liver tissue and blood were harvested after 8 weeks (rats) and 2 weeks (mice), which were detected by TG, CHO, FPG, FINS, HE and oil-red O. At last, the rats were assessed by NAFLD Activity Score (NAS) and HOMA-IR. Results: The levels of serum TG, CHO, FPG, FINS, HOMA-IR were significantly increased in NASH rats. The levels of serum TG, CHO were significantly decreased in NASH mice. The results of HE, oil-red O and NAS show liver tissue of rats and mice have been developed to NASH. Conclusion: Two methods can be simulated human NASH disease in serology and pathology, high-fat diet induced by NASH model can simulate the process and mechanism of human NASH disease, and this model can copy insulin resistance and oxidative stress, so this method have more advantage in NASH research field.
Keywords:Non-alcoholic steatohepatitis  Animal model  Comparison  Serology  Pathology
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