扑热息痛肝损伤机制研究进展

被引:30
作者
顾兴丽
孙继红
季晖
机构
[1] 中国药科大学药理教研室
关键词
扑热息痛肝毒性; 氧化应激; 线粒体功能异常; 炎症介质;
D O I
暂无
中图分类号
R575 [肝及胆疾病]; R595.3 [药源性疾病];
学科分类号
100201 [内科学];
摘要
扑热息痛(AAP)肝损伤是药物性肝损伤的常见原因之一。但迄今为止,其肝损伤机制仍不完全清楚。最新研究进展指出活性代谢产物的形成、谷胱甘肽的耗竭、线粒体蛋白的烷化和过氧化亚硝酸盐的形成是主要原因。本文主要描述了AAP过量所致的线粒体功能异常的研究进展,另外也综述了氧化应激和炎症介质在扑热息痛肝损伤机制中的作用。
引用
收藏
页码:596 / 600
页数:5
相关论文
共 11 条
[1]
药物性肝病 [J].
李岩 .
中国实用内科杂志, 2006, (21) :1669-1672
[2]
Oxidative stress and monooxygenase liver function in patients with coronary heart disease and multiple organ dysfunction syndrome [J].
Nepomniashchikh, V. A. ;
Lomivorotov, V. V. ;
Deryagin, M. N. ;
Lomivorotov, V. N. ;
Kniazkova, L. G. .
EUROPEAN JOURNAL OF ANAESTHESIOLOGY, 2009, 26 (02) :140-146
[3]
Mitochondrial protein thiol modifications in acetaminophen hepatotoxicity: Effect on HMG-CoA synthase [J].
Andringa, Kelly K. ;
Bajt, Mary Lynn ;
Jaeschke, Hartmut ;
Bailey, Shannon M. .
TOXICOLOGY LETTERS, 2008, 177 (03) :188-197
[4]
Role of nitric oxide and reduced glutathione in the protective effects of aminoguanidine; gadolinium chloride and oleanolic acid against acetaminophen-induced hepatic and renal damage.[J].Ahmed O. Abdel-Zaher;Mahmoud M. Abdel-Rahman;Moumen M. Hafez;Faten M. Omran.Toxicology.2007, 1
[5]
Leflunomide or A77 1726 protect from acetaminophen-induced cell injury through inhibition of JNK-mediated mitochondrial permeability transition in immortalized human hepatocytes [J].
Latchoumycandane, Calivarathan ;
Seah, Quee Ming ;
Tan, Rachel C. H. ;
Sattabongkot, Jetsumon ;
Beerheide, Walter ;
Boelsterli, Urs A. .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 2006, 217 (01) :125-133
[6]
Liquiritigenin, an aglycone of liquiritin in Glycyrrhizae radix, prevents acute liver injuries in rats induced by acetaminophen with or without buthionine sulfoximine [J].
Kim, Young Woo ;
Ki, Sung Hwan ;
Lee, Jong Rok ;
Lee, Song Jin ;
Kim, Choon Won ;
Kim, Sang Chan ;
Kim, Sang Geon .
CHEMICO-BIOLOGICAL INTERACTIONS, 2006, 161 (02) :125-138
[7]
Exaggerated hepatic injury due to acetaminophen challenge in mice lacking C-C chemokine receptor 2 [J].
Hogaboam, CM ;
Bone-Larson, CL ;
Steinhauser, ML ;
Matsukawa, A ;
Gosling, J ;
Boring, L ;
Charo, IF ;
Simpson, KJ ;
Lukacs, NW ;
Kunkel, SL .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 156 (04) :1245-1252
[8]
A hepatotoxic dose of acetaminophen modulates expression of BCL-2, BCL-XL, and BCL-XS during apoptotic and necrotic death of mouse liver cells in vivo [J].
Sidhartha D. Ray ;
Nilameni Jena .
Archives of Toxicology, 2000, 73 :594-606
[9]
Deferoxamine delays the development of the hepatotoxicity of acetaminophen in mice [J].
Schnellmann, JG ;
Pumford, NR ;
Kusewitt, DF ;
Bucci, TJ ;
Hinson, JA .
TOXICOLOGY LETTERS, 1999, 106 (01) :79-88
[10]
Protection in the late stages of paracetamol-induced liver cell injury with fructose, cyclosporin A and trifluoperazine [J].
Beales, D ;
McLean, AEM .
TOXICOLOGY, 1996, 107 (03) :201-208