对乙酰氨基酚肝毒性机制与防治研究新进展  

Progress in mechanism of acetaminophen-induced hepatotoxicity and its protective strategies

作　　者：潘家琪[1] 宋丹军 李鹏旭 刘爱明[1] 

机构地区：[1]宁波大学医学院生理药理学系,浙江宁波315211

出　　处：《中国药理学与毒理学杂志》2014年第4期618-624,共7页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金(81273582);国家自然科学基金(81302848);浙江省自然科学基金(Y2110016)~~

摘　　要：对乙酰氨基酚(APAP)(扑热息痛)是临床应用最广泛的解热镇痛药,也是引起肝功能衰竭最常见的药物。作为肝毒性模型工具药物,APAP也被广泛用于药物肝毒性机制研究和药物护肝作用评价。本文对APAP肝毒性中代谢活化、细胞损伤、c-Jun N端激酶信号通路和代谢功能改变等细胞内事件,炎症细胞与炎症因子在APAP肝毒性中的作用,以及单体化合物和天然提取物对抗APAP肝毒性的研究进展进行综述,为其肝毒性的发生机制和防治研究提供参考。Acetaminophen （APAP） is the most widely-used analgesic drug clinically. It is also the most risky agent for hepatotoxicity. It has been widely used as a model drug to study mechanisms of chemical-induced liver injury and to test the hepatoprotective potential of chemicals. This review summa- rized the intracellular events of acetaminophen-induced hepatotoxicity, including metabolic activation, cellular damage, c-Jun N-terminal kinase pathway, and modified metabolism function, and additionally focused on the role of inflammatory factors and cells in APAP hepatotoxicity, as well as protection strate- gies of chemicals and natural products.

关 键 词：对乙酰氨基酚 药物毒性 肝 炎症 

分 类 号：R994.3[医药卫生—毒理学]