对乙酰氨基酚损伤肝线粒体造成肝衰竭的分子机制及应用

Molecular Mechanism and Application of Acetaminophen-induced Hepatic Failure through Hepatic Mitochondrial Damage

对乙酰氨基酚是临床上常用的解热镇痛药,但也是造成药物性肝损伤最多的药物。目前认为对乙酰氨基酚导致肝损伤的机制涉及氧化应激、线粒体损伤、炎症等多个方面。已有研究显示线粒体是对乙酰氨基酚造成肝损伤的重要靶点,从线粒体损伤出发,结合代谢与免疫阐述对乙酰氨基酚通过代谢产物破坏线粒体结构和功能并激活肝脏免疫应答造成肝脏受损的分子机制,并以抗氧化和修复损伤线粒体为基础,探讨对乙酰氨基酚肝毒性的潜在治疗方法。

Acetaminophen,which is a very commonly used antipyretic and analgesic medicine in clinical practice,can easily induce liver injury.It is generally thought that the mechanism of acetaminophen-induced liver injury involves oxidative stress,mitochondrial damage,inflammation,etc..Researches show that mitochondria is an important target for acetaminophen-induced liver damage.From the perspective of metabolism and immunity,this paper attempts to uncover the molecular mechanism of acetaminophen in hepatic injury from destruction of mitochondrial structure and function through the metabolites of acetaminophen and activation of liver immune response,with an exploration of the potential therapeutic methods based on antioxidation and repair of damaged mitochondria.