文献类型：期刊文献

英文题名：Pharmacodynamic material basis of licorice and mechanisms of modulating bile acid metabolism and gut microbiota in cisplatin-induced liver injury based on LC-MS and network pharmacology analysis

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

第一作者：李俊

通信作者：Deng, Y[1];Yang, ZJ[1];Yang, XJ[1]

机构：[1]Gansu Univ Tradit Chinese Med, Sch Pharmaceut Sci, Lanzhou 730000, Peoples R China;[2]Shaanxi Univ Chinese Med, Xian 712046, Peoples R China;[3]Qinghai Univ, Fac Med, Xining 810016, 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 730000, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：340

外文期刊名：JOURNAL OF ETHNOPHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-85213556773);WOS:【SCI-EXPANDED(收录号:WOS:001421851100001)】；

基金：This study was supported by the National Natural Science Founda-tion of China (No. 81960723) , Lanzhou Science and Technology Pro-gram (No. 2022-3-21) , Gansu Provincial Administration of Traditional Chinese Medicine (No. GZKP-2022-37) , Gansu Provincial Natural Sci-ence Foundation (No. 21JR11RA145; No. 22JR11RA112) , and Gansu Provincial Traditional Chinese Medicine Concocting Technology Inher-itance Base Project.

语种：英文

外文关键词：Licorice; Hepatotoxicity; Cisplatin; Bile acid metabolism; Gut microbiota

摘要：Ethnopharmacological relevance: Cisplatin (CP), a widely used antineoplastic agent, is a leading cause of drug- induced liver injury (DILI) due to its hepatotoxic effects. Licorice (GC), an established remedy in traditional Chinese medicine (TCM), has shown promise in addressing liver diseases and DILI. Nonetheless, the specific active components and underlying mechanisms of GC in mitigating CP-induced liver injury remain inadequately investigated. Aim of the study: This study examined the active components and efficacy of GC in addressing CP-induced hepatotoxicity, focusing on its mechanisms related to bile acid metabolism and gut microbiota regulation. Materials and methods: Utilizing a CP-induced rat liver injury model, this study evaluated changes in liver coefficient, liver function indices, and pathological morphology while assessing the efficacy of GC for both prevention and treatment of CP-induced liver injury. Subsequently, UPLC-Q-TOF-MS qualitatively analyzed GC's blood-entering components, elucidating its pharmacodynamic material basis. Network pharmacology analysis identified potential pathways and targets of GC's blood components in relation to CP-induced liver injury. Furthermore, metabolomics and 16S rRNA sequencing were employed to clarify the pharmacodynamic mechanisms of GC in modulating bile acid metabolism and gut microbiota, offering insights into its preventive and therapeutic roles. Results: The pharmacodynamic results revealed that GC significantly reduced liver function biomarkers and improved pathological changes in liver tissue. UPLC-Q-TOF-MS analysis identified 16 blood-entering components as potential pharmacodynamic agents of GC for preventing and treating CP-induced liver injury. Network pharmacology analysis suggested a link between GC's efficacy and the bile acid metabolic pathway. Furthermore, metabolomics analysis, immunoblotting, and 16S rRNA sequencing demonstrated that GC regulated bile acid metabolites in both liver and feces, enhanced FXR and BSEP expressions in the liver, and decreased CYP27A1 expression. Additionally, GC mitigated CP-induced intestinal dysbiosis by altering the abundance of gut microbiota. Conclusions: UPLC-Q-TOF-MS performed a qualitative analysis of 16 blood-entering components linked to GC, providing a basis for further exploration of the pharmacodynamic material underpinning GC. The protective role of GC in CP-induced liver injury appears connected to enhanced bile acid metabolism and restoration of gut microbiota balance.