Application of HepG2-derived organoid and organ-on-a-chip platforms in elucidating selenium-mediated protection against cadmium-induced liver dysfunction

npj Science of Food 2026 Open access

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Authors: Meng Ren, Qing Feng, Surui Lu, W C Xiao, Qihong Deng, X William Yang, Cheng Zeng Yan, Zhanhong Ren, Biao Yan, Yang Wu, Shaodan Huang, X William Yang
+2 more Ping Ma, Liqin Su
DOI: 10.1038/s41538-025-00669-4
Cited by: 1
References: 36

Abstract

HepG2 cells were cultured into liver organoids (more native liver-like than 2D cultures) and integrated into a microfluidic chip, which regulates flow, nutrients, and waste to simulate in vivo hepatic microcirculation. Key findings: Cadmium (Cd) exposure shows a positive dose-response with liver damage; 40 ng/mL selenium (Se) alleviates 3 sets of liver biochemical dysfunctions under 40 μg/mL Cd co-exposure, but 160/640 ng/mL Se diminishes this protection. Metabolomics (40 μg/mL Cd vs. 640 ng/mL Se+Cd) identified two mechanisms: high Se induces oxidative stress and disrupts liver cellular metabolism. This study provides data/theory for rational Se use against Cd-induced liver dysfunction. The platform integrates organoid/organ-on-a-chip assessments with microfluidic metabolomics (a cross-scale toxicological system) and informs 3D cell model development.

Fields of Study & Subjects

Liver physiology and pathology 3D Printing in Biomedical Research Pluripotent Stem Cells Research

Publication details

Journal / source
npj Science of Food
Publisher
Springer Science and Business Media LLC
Volume
10
Issue
1
Pages
22–22
Publication date
6 January 2026
Language
EN