文献类型：期刊文献

英文题名：Licorice attenuates cisplatin-induced hepatotoxicity by alleviating endoplasmic reticulum stress and apoptosis

作者：Li, Jie[1];Yang, Xiujuan[1];Lian, Xiaolong[2];Li, Baojian[3];Ma, Quhuan[1];Yang, Lingling[1];Gao, Guangmiao[1];Deng, Yi[1];Yang, Zhijun[1]

第一作者：李俊

通信作者：Deng, Y[1];Yang, ZJ[1]

机构：[1]Gansu Univ Tradit Chinese Med, Sch Pharmaceut Sci, Lanzhou, Gansu, Peoples R China;[2]Qinghai Univ, Med Coll, Dept Pharm, Xining, Peoples R China;[3]Shaanxi Univ Chinese Med, Xian, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Tradit Chinese Med, Sch Pharmaceut Sci, Lanzhou, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：16

外文期刊名：FRONTIERS IN PHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-105001654029);WOS:【SCI-EXPANDED(收录号:WOS:001457590200001)】；

基金：The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by the National Natural Science Foundation of China (No. 81960723), Lanzhou Science and Technology Program (No. 2022-3-21), Gansu Provincial Administration of Traditional Chinese Medicine (No. GZKP-2022-37), Gansu Provincial Natural Science Foundation (No. 21JR11RA145; No. 22JR11RA112), and Gansu Provincial Traditional Chinese Medicine Concocting Technology Inheritance Base Project.

语种：英文

外文关键词：licorice; hepatotoxicity; ER stress; PERK/ATF4/CHOP pathway; apoptosis

摘要：Cisplatin (CP), a widely used antineoplastic drug, could induce hepatotoxicity and is also one of the most common reasons for drug-induced liver injury (DILI). Licorice (Chinese name GanCao, GC) is a commonly used herbal drug in traditional Chinese medicine (TCM) that has been shown to treat liver diseases and DILI. CP has been documented to induce apoptosis through the promotion of endoplasmic reticulum (ER) stress. However, the exact role of ER stress in the pathogenesis of CP-induced hepatotoxicity remains unclear. A rat DILI model was constructed through intraperitoneal injection of CP, and the anti-DILI effect of GC was detected by liver coefficients, liver function tests, pathological staining, and oxidative stress indices. Additionally, the ER stress and apoptosis indices were investigated by quantitative real-time PCR (qRT-PCR), Western blotting, and immunofluorescence (IF) on CP-induced toxicity in rat liver tissues and LO2 cells. In the model group, liver function indicators significantly elevated, liver lesions more pronounced, and the reactive oxygen species (ROS) level in the liver increased, the expression of ER stress markers, apoptosis factors, and indicators related to the protein kinase RNA-like ER kinase/activating transcription factor 4/C/EBP homologous protein (PERK/ATF4/CHOP) pathway significantly elevated. Treatment of the CP-induced toxicity in the rat model with GC significantly improved liver function, reduced liver lesions, decreased liver ROS. In addition, GC significantly inhibited the expression of ER stress markers, apoptosis factors, and indicators related to PERK/ATF4/CHOP pathway, demonstrating the anti-CP-induced hepatotoxicity effect of GC. In this study, we verified the protective effect of GC in CP-induced hepatotoxicity in rats and clarified its mechanisms related to ER stress and apoptosis.