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Liberation of daidzein by gut microbial β-galactosidase suppresses acetaminophen-induced hepatotoxicity in mice

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机构： [1]Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China [3]Guangdong Provincial Key Laboratory of Proteomics, State Key Laboratory of Organ Failure Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China [4]Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education, Guangdong Pharmaceutical University, Guangzhou 510006, China [5]Institute of Ecological Science, School of Life Science, South China Normal University, Guangzhou 510631, China [6]Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510120, China [7]Department of Critical Care Medicine, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510665, China [8]Department of Obstetrics and Gynecology, First People’s Hospital of Foshan, Foshan 528000, China

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Acetaminophen (APAP) overdose is a leading cause of drug-induced liver injury (DILI). The impact of the gut microbiota and associated metabolites on APAP and liver function remains unclear. We show that APAP disturbance is associated with a distinct gut microbial community, with notable decreases in Lactobacillus vaginalis. Mice receiving L. vaginalis showed resistance to APAP hepatotoxicity due to the liberation of the isoflavone daidzein from the diet by bacterial β-galactosidase. The hepatoprotective effects of L. vaginalis in APAP-exposed germ-free mice were abolished with a β-galactosidase inhibitor. Similarly, β-galactosidase-deficient L. vaginalis produced poorer outcomes in APAP-treated mice than the wild-type strain, but these differences were overcome with daidzein administration. Mechanistically, daidzein prevented ferroptotic death, which was linked to decreased expression of farnesyl diphosphate synthase (Fdps) that activated a key ferroptosis pathway involving AKT-GSK3β-Nrf2. Thus, liberation of daidzein by L. vaginalis β-galactosidase inhibits Fdps-mediated hepatocyte ferroptosis, providing promising therapeutic approaches for DILI.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

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出版当年[2022]版：

大类 | 1 区

医学

小类 | 1 区微生物学 1 区寄生虫学 1 区病毒学

最新[2025]版：

大类 | 1 区

医学

小类 | 1 区微生物学 1 区寄生虫学 1 区病毒学

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第一作者机构： [1]Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China

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通讯机构： [1]Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China [3]Guangdong Provincial Key Laboratory of Proteomics, State Key Laboratory of Organ Failure Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China

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