扑热息痛肝毒性中炎症反应的研究进展

Progress of Inflammation in Liver Toxicity Caused by Acetaminophen

扑热息痛(N-acetyl-para-aminophenol,APAP)是临床应用最广泛的解热镇痛药;作为肝毒性工具药物,APAP也被广泛用于药物肝毒性机制研究和测试药物的护肝潜力。炎症是加重细胞损伤的一个潜在因素,也能限制细胞损伤,清除细胞碎片和促进再生。30余年来,APAP肝毒性机制的研究和讨论一直在持续。笔者针对APAP肝毒性中的细胞内事件,尤其是与炎症反应、炎症介质、炎症细胞之间的关系进行综述,为临床应用和毒性机制研究提供参考。

As the most widely used antipyretic analgesic, acetaminophen has been widely used as a model drug to study mechanisms of chemical-induced liver toxicity and test hepato-protective potential of new drugs. Inflammation may aggravate cell damage, by limiting cell injury, removing cell debris and promoting regeneration. The mechanisms of AAP-induced liver cell injury have been extensively investigated and discussed for more than 30 years. This review focuses on the intracellular events of acetaminophen-induced hepatotoxicity, particularly the relevance of the inflammatory response, inflammatory mediators and inflammatory cells, to help improve clinical application and lay a good basis for mechanism investigation.