Pharmacological mechanisms of quercetin in liver and intestinal diseases: a gut-liver axis perspective
- 1Graduate School, Tianjin University of Traditional Chinese Medicine , ,
- 2School of Pharmacy, Shandong University of Traditional Chinese Medicine , ,
- 3Lunan Pharmaceutical Group Co., Ltd. , ,
Abstract
Hepatic and gastrointestinal disorders share interconnected pathogenic mechanisms, yet their clinical management remains challenging. This has prompted interest in therapeutic approaches targeting the gut-liver axis. Quercetin, a natural flavonoid, has been studied in this context. To assess its pharmacological effects, we searched PubMed, Web of Science, EMBASE, and the Cochrane Library for literature published since 2000 on quercetin in hepatic and intestinal diseases. This review focuses on the gut-liver axis as a framework for understanding the pharmacological effects of quercetin. Mechanistically, quercetin modulates gut-liver communication by reshaping the gut microbiota, promoting short-chain fatty acid production, and modulating bile acid metabolism. In preclinical models, it has been reported to modulate FXR/TGR5 signaling and preserve intestinal barrier integrity, thereby reducing endotoxin translocation and systemic inflammation. These effects are associated with downstream modulation of oxidative, inflammatory, and apoptotic pathways, including NF-κB, PI3K/Akt, and Nrf2. Furthermore, preclinical evidence indicates that quercetin attenuates liver injury, MASLD/MASH, fibrosis, and hepatocellular carcinoma, and exerts protective effects in models of ulcerative colitis and colorectal cancer. However, most of this evidence comes from in vitro and animal studies, and clinical evidence remains limited. By focusing on gut-liver crosstalk, this review provides a framework for understanding the pharmacological effects of quercetin and identifies key gaps that need to be addressed before clinical translation can be considered.
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BibTeX
@article{he2026pharmacological,
title = {{Pharmacological mechanisms of quercetin in liver and intestinal diseases: a gut-liver axis perspective}},
author = {Xiaozhong He and Tianyi Zhang and Yanqi Li and Yunshun Qiu and Chun Wang and Hui Wang and Liyuan Liu and Yihuan Wang and Guimin Zhang and Zhong Feng},
journal = {Frontiers in pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1958426},
url = {https://europepmc.org/article/PMC/PMC13669718},
note = {CC BY},
}
RIS
TY - JOUR
TI - Pharmacological mechanisms of quercetin in liver and intestinal diseases: a gut-liver axis perspective
AU - Xiaozhong He
AU - Tianyi Zhang
AU - Yanqi Li
AU - Yunshun Qiu
AU - Chun Wang
AU - Hui Wang
AU - Liyuan Liu
AU - Yihuan Wang
AU - Guimin Zhang
AU - Zhong Feng
PY - 2026
DA - 2026/10/01
JO - Frontiers in pharmacology
DO - 10.3389/fphar.2026.1958426
UR - https://europepmc.org/article/PMC/PMC13669718
AB - Hepatic and gastrointestinal disorders share interconnected pathogenic mechanisms, yet their clinical management remains challenging. This has prompted interest in therapeutic approaches targeting the gut-liver axis. Quercetin, a natural flavonoid, has been studied in this context. To assess its pharmacological effects, we searched PubMed, Web of Science, EMBASE, and the Cochrane Library for literature published since 2000 on quercetin in hepatic and intestinal diseases. This review focuses on the gut-liver axis as a framework for understanding the pharmacological effects of quercetin. Mechanistically, quercetin modulates gut-liver communication by reshaping the gut microbiota, promoting short-chain fatty acid production, and modulating bile acid metabolism. In preclinical models, it has been reported to modulate FXR/TGR5 signaling and preserve intestinal barrier integrity, thereby reducing endotoxin translocation and systemic inflammation. These effects are associated with downstream modulation of oxidative, inflammatory, and apoptotic pathways, including NF-κB, PI3K/Akt, and Nrf2. Furthermore, preclinical evidence indicates that quercetin attenuates liver injury, MASLD/MASH, fibrosis, and hepatocellular carcinoma, and exerts protective effects in models of ulcerative colitis and colorectal cancer. However, most of this evidence comes from in vitro and animal studies, and clinical evidence remains limited. By focusing on gut-liver crosstalk, this review provides a framework for understanding the pharmacological effects of quercetin and identifies key gaps that need to be addressed before clinical translation can be considered.
SN - 1663-9812
ER -