背景介绍：

药物性肝损伤（drug induced liver injury，DILI）可分为固有型与特异质两类，是导致新药撤市、急性肝衰竭的主要诱因。其中过量服用对乙酰氨基酚（APAP）引发的固有型肝损伤，占欧美地区急性肝衰竭病例半数以上。APAP经CYP2E1催化生成毒性代谢物N-乙酰对苯醌亚胺（NAPQI），大量耗竭肝细胞谷胱甘肽（GSH），直接诱发肝细胞损伤；同时机体固有免疫稳态失衡，进一步加重肝组织坏死。采用APAP诱导构建小鼠肝损伤模型可稳定复刻该完整损伤通路，既是研究药物肝毒性、筛选保肝干预手段的经典动物模型，也可为解析特异质肝损伤的共有病理机制提供重要研究载体。^[1-2]

图1. 实验性对乙酰氨基酚（APAP）肝毒性的当前研究理论 ^[1]

APAP诱导动物肝损伤模型参考：^[2-5]

造模成功关键指标：血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）水平显著升高。

药物性肝损伤模型1相关产品推荐：

参考文献：

[1] Kaplowitz Neil. Idiosyncratic Drug Hepatotoxicity. Nature Reviews Drug Discovery, vol. 4, no. 6, 2005, pp. 489–499.

[2] Eakins R., et al. Adaptation to acetaminophen exposure elicits major changes in expression and distribution of the hepatic proteome. Scientific Reports, vol. 5, 2015, p. 16423.

[3] Bi Jianbin, et al. HSF2BP protects against acute liver injury by regulating HSF2/HSP70/MAPK signaling in mice. Cell Death & Disease, vol. 13, no. 9, 2022, p. 830.

[4] Yang Hanyu, et al. Acute liver failure-induced arginine deficiency impairs blood-brain barrier via inhibiting mTORC1-S6K1/4EBP1 pathway and inducing autophagy. Cell Death & Disease, vol. 16, no. 11, 2025, p. 842.

[5] Wu Bao, et al. Hepatic SNHG9 links gut microbiota to liver protection in drug-induced liver injury. Nature Communications, vol. 17, 2026, p. 4415.