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Animal Models Correlating Immune Cells for the Development of NAFLD/NASH.与非酒精性脂肪性肝病/非酒精性脂肪性肝炎发展相关的免疫细胞的动物模型
J Clin Exp Hepatol. 2015 Sep;5(3):239-45. doi: 10.1016/j.jceh.2015.06.004. Epub 2015 Jul 9.
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CD44 is a key player in non-alcoholic steatohepatitis.CD44 是非酒精性脂肪性肝炎的关键参与者。
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Mitochondrial gene polymorphisms alter hepatic cellular energy metabolism and aggravate diet-induced non-alcoholic steatohepatitis.线粒体基因多态性改变肝脏细胞能量代谢并加重饮食诱导的非酒精性脂肪性肝炎。
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A Cholecystokinin Receptor Antagonist Halts Nonalcoholic Steatohepatitis and Prevents Hepatocellular Carcinoma.一种胆囊收缩素受体拮抗剂可阻止非酒精性脂肪性肝炎并预防肝细胞癌。
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本文引用的文献

1
B cell-activating factor is associated with the histological severity of nonalcoholic fatty liver disease.B细胞活化因子与非酒精性脂肪性肝病的组织学严重程度相关。
Hepatol Int. 2013 Jun;7(2):539-47. doi: 10.1007/s12072-012-9345-8. Epub 2012 Feb 9.
2
Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes.肝内 CD8+T 细胞和 NKT 细胞的代谢激活通过与肝细胞的交叉对话导致非酒精性脂肪性肝炎和肝癌。
Cancer Cell. 2014 Oct 13;26(4):549-64. doi: 10.1016/j.ccell.2014.09.003.
3
IL-1 signaling in obesity-induced hepatic lipogenesis and steatosis.白细胞介素-1在肥胖诱导的肝脏脂肪生成和脂肪变性中的信号传导
PLoS One. 2014 Sep 12;9(9):e107265. doi: 10.1371/journal.pone.0107265. eCollection 2014.
4
Protective role of macrophage migration inhibitory factor in nonalcoholic steatohepatitis.巨噬细胞移动抑制因子在非酒精性脂肪性肝炎中的保护作用
FASEB J. 2014 Dec;28(12):5136-47. doi: 10.1096/fj.14-256776. Epub 2014 Aug 13.
5
Chemokine-like receptor 1 deficiency does not affect the development of insulin resistance and nonalcoholic fatty liver disease in mice.趋化因子样受体1缺乏不影响小鼠胰岛素抵抗和非酒精性脂肪性肝病的发展。
PLoS One. 2014 Apr 29;9(4):e96345. doi: 10.1371/journal.pone.0096345. eCollection 2014.
6
Immune and inflammatory pathways in NASH.非酒精性脂肪性肝炎中的免疫和炎症途径。
Hepatol Int. 2013 Aug 30;7 Suppl 2(Suppl 2):771-81. doi: 10.1007/s12072-013-9468-6. eCollection 2013 Dec.
7
Mice lacking natural killer T cells are more susceptible to metabolic alterations following high fat diet feeding.缺乏自然杀伤T细胞的小鼠在高脂饮食喂养后更容易出现代谢改变。
PLoS One. 2014 Jan 20;9(1):e80949. doi: 10.1371/journal.pone.0080949. eCollection 2014.
8
Role of immunodeficient animal models in the development of fructose induced NAFLD.免疫缺陷动物模型在果糖诱导的非酒精性脂肪性肝病发展中的作用。
J Nutr Biochem. 2014 Feb;25(2):219-26. doi: 10.1016/j.jnutbio.2013.10.010. Epub 2013 Nov 18.
9
IL-17 signaling accelerates the progression of nonalcoholic fatty liver disease in mice.IL-17 信号通路加速了小鼠非酒精性脂肪性肝病的进展。
Hepatology. 2014 May;59(5):1830-9. doi: 10.1002/hep.26746. Epub 2014 Mar 27.
10
Neutralization of interleukin-17 attenuates high fat diet-induced non-alcoholic fatty liver disease in mice.白细胞介素-17 的中和作用可减轻高脂饮食诱导的小鼠非酒精性脂肪性肝病。
Acta Biochim Biophys Sin (Shanghai). 2013 Sep;45(9):726-33. doi: 10.1093/abbs/gmt065. Epub 2013 Jun 19.

与非酒精性脂肪性肝病/非酒精性脂肪性肝炎发展相关的免疫细胞的动物模型

Animal Models Correlating Immune Cells for the Development of NAFLD/NASH.

作者信息

Iyer Srikanth, Upadhyay Pramod Kumar, Majumdar Subeer S, Nagarajan Perumal

机构信息

National Institute of Immunology, New Delhi 110067, India.

出版信息

J Clin Exp Hepatol. 2015 Sep;5(3):239-45. doi: 10.1016/j.jceh.2015.06.004. Epub 2015 Jul 9.

DOI:10.1016/j.jceh.2015.06.004
PMID:26628841
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4632099/
Abstract

This review mainly elaborates on the animal models available for understanding the pathogenesis of the second hit of non-alcoholic fatty liver disease (NAFLD) involving immune system. This is known to be a step forward from simple steatosis caused during the first hit, which leads to the stage of inflammation followed by more serious liver conditions like non-alcoholic steatohepatitis (NASH) and cirrhosis. Immune-deficient animal models serve as an important tool for understanding the role of a specific cell type or a cytokine in the progression of NAFLD. These animal models can be used in combination with the already available animal models of NAFLD, including dietary models, as well as genetically modified mouse models. Advancements in molecular biological techniques enabled researchers to produce several new animal models for the study of NAFLD, including knockin, generalized knockout, and tissue-specific knockout mice. Development of NASH/NAFLD in various animal models having compromised immune system is discussed in this review.

摘要

本综述主要阐述了可用于理解涉及免疫系统的非酒精性脂肪性肝病(NAFLD)二次打击发病机制的动物模型。众所周知,这是从首次打击期间引起的单纯脂肪变性向前迈出的一步,单纯脂肪变性会导致炎症阶段,进而发展为更严重的肝脏疾病,如非酒精性脂肪性肝炎(NASH)和肝硬化。免疫缺陷动物模型是理解特定细胞类型或细胞因子在NAFLD进展中作用的重要工具。这些动物模型可与现有的NAFLD动物模型(包括饮食模型以及基因改造小鼠模型)结合使用。分子生物学技术的进步使研究人员能够制备多种用于研究NAFLD的新动物模型,包括敲入小鼠、全身性敲除小鼠和组织特异性敲除小鼠。本综述讨论了免疫系统受损的各种动物模型中NASH/NAFLD的发展情况。