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作 者:岳淑雯 陈真[1] YUE Shuwen;CHEN Zhen(College of Pharmacy,China Pharmaceutical University,Nanjing 211198,China)
出 处:《药学研究》2019年第1期49-52,共4页Journal of Pharmaceutical Research
摘 要:肝脏具有物质合成、解毒和抗氧化等多种功能,同时也易于受到自由基和某些药物的攻击而产生损伤。肝脏疾病一直是临床研究的重点,而急性肝损伤是几乎所有肝脏疾病的开端。目前已有多种动物模型可以分别模仿不同发病机制的急性肝损伤,针对不同发病机制的通路研究也在不断进行。本文简述了四氯化碳(CCl4)、半乳糖胺/脂多糖(D-Gal N/LPS)、对乙酰氨基酚和酒精介导的急性肝损伤模型,并简要介绍了Kelch样ECH相关蛋白1(Keap1)-核因子E2相关蛋白2(Nrf2)、Toll样受体4(TLR4)和NLRP3通路在急性肝损伤发生发展进程中的作用。Liver has the function of synthesis,detoxify,antioxidant activity,etc.Meanwhile it is liable to be attacked by free radical and some drugs.Liver diseases have always been the center of clinical researcher,while acute liver injury is the initiating condition of almost all liver diseases with diverse pathogenesis.There have been many kinds of animal models simulating different injury types,following with three signaling pathway associated with acute liver injury.Here we sketched four common animal models,among which are CCl 4,D-GalN/LPS,APAP and alcohol,and introduced the roles of three signaling pathways,Keap1-Nrf2,TLR4 and NLRP3,in the development and progression of acute liver injury.
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