Evidence map›Paper›PMID 41066001›Full record

ArticleMolecular biology reports2025

Naringin mitigates liver damage in a tissue-engineered liver of metabolic dysfunction-associated steatotic liver disease model by promoting autophagy via the mTOR-ULK1 pathway.

Jihui Jia, Yizhi Zhang, Jing Lin, Zhongping Duan, Yu Chen, Xiaohui Zhang

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Jihui Jia *Beijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Yizhi Zhang *Department of critical liver diseases, Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Jing LinFourth Department of Liver Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Zhongping DuanFourth Department of Liver Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Yu ChenFourth Department of Liver Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Xiaohui ZhangFourth Department of Liver Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, China. xiaohui.zhang@ccmu.edu.cn.

Funding

Beijing Institute of Hepatology Reform and Development Project 2024Y-KF-08; 2025Y-KF-Q08Beijing Natural Science Foundation 7202070Beijing You'an Hospital Construction of Talent Pool Program YARCKC2022004Construction Project of High-level Technology Talents in Public Health Discipline backbone-02-24National Natural Science Foundation of China 82470606Open Research Project of Beijing Key Laboratory of Beijing Youan Hospital Affiliated to Capital Medical University BJYAHKF2023003
6 · The paper itself

Abstract

backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver disease with complex pathogenesis. Autophagy is involved in the occurrence and development of MASLD. Naringin is a flavonoid compound with anti-inflammatory and anti-oxidation effects. This study is to investigate the impact of naringin on autophagy in an organoid model of tissue-engineered fatty liver (TEF). METHODS AND

resultsHuman hepatocytes were cultured on a rat liver biomatrix scaffold and perfused with fat-supplemented medium to establish 3D MASLD models. Naringin was treated for 3 days. Histopathological changes were determined by oil red O and hematoxylin-eosin staining; organelle morphology was examined by scanning electron microscopy and transmission electron microscopy (TEM); the expression of autophagy-related factors was analyzed by qPCR and Western Blot. Hepatocyte injury was determined by terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) staining, cell counting and lactate dehydrogenase (LDH) detection. The results showed naringin significantly improved liver injury in the MASLD model, as evidenced by increased cell viability, reduced lipid accumulation and LDH release. TEM revealed the presence of autophagosomes in naringin-treated hepatocytes. Naringin upregulated the expression of autophagy-related proteins (LC3, ATG5, ATG7) and promoted the LC3-II/LC3-I ratio, indicating enhanced autophagic flux. Furthermore, naringin regulated the mTOR-ULK1 signaling pathway by downregulating p-mTOR and p-ULK1 (Ser757) and upregulating Beclin1. Autophagy inhibitors (3-Methyladenine and SBI-0206965) attenuated the protective effects of naringin, confirming the role of autophagy in hepatocyte protection.

conclusionNaringin mitigates liver damage in the TEF model by enhancing autophagy via mTOR-ULK1 pathway, highlighting its potential as a therapeutic agent for MASLD.

Indexed as

AutophagyAutophagy-Related Protein-1 HomologFatty LiverFlavanonesTOR Serine-Threonine KinasesAnimalsDisease Models, AnimalHepatocytesHumansIntracellular Signaling Peptides and ProteinsLiverMaleRatsRats, Sprague-DawleySignal TransductionAutophagy-Related Protein-1 HomologFlavanonesIntracellular Signaling Peptides and ProteinsnaringinTOR Serine-Threonine KinasesULK1 protein, humanAutophagyMetabolic dysfunction-associated steatotic liver diseaseNaringinOrganoidTissue-engineered liver

Identifiers

PMID41066001

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.