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Updated: May 14, 2026

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Published on: January 31, 2022

Tripterygium Glycosides Extract-Induced Hepatic Cholestasis: A Mechanistic Study Using a Microfluidic Liver-on-a-Chip

Yifei Yang¹, Ya Zhang¹, Yun Yang¹

¹Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, State Key Laboratory for Quality Ensurance and Sustainable Use of Dao-di Herbs, Beijing 100700, China.

International Journal of Molecular Sciences

|May 13, 2026

Summary

Tripterygium glycosides extract (TGE) causes cholestatic liver injury by triggering oxidative stress and inflammation, which suppresses bile acid transport. This study used a liver-on-a-chip model to reveal TGE

Keywords:

bile acid transporters drug-induced liver injury farnesoid X receptor oxidative stress precision-cut liver slices

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An Intestine/Liver Microphysiological System for Drug Pharmacokinetic and Toxicological Assessment

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Published on: December 3, 2020

Area of Science:

Hepatology
Toxicology
Biomaterials

Background:

Tripterygium glycosides extract (TGE) is used for immune disorders but linked to cholestatic liver injury.
Traditional models struggle to replicate complex Chinese medicine toxicity mechanisms.

Purpose of the Study:

To elucidate the mechanisms of TGE-induced cholestatic liver injury.
To utilize a biomimetic microfluidic liver-on-a-chip platform for studying TGE toxicity.

Main Methods:

A liver-on-a-chip platform integrating rat precision-cut liver slices and human endothelial cells was developed.
Exposure to TGE at varying concentrations and durations (15-135 μg/mL for 12 and 24 h).
Assessment of liver injury markers, oxidative stress, inflammatory cytokines, and bile acid transporter expression.

Main Results:

TGE exposure significantly increased liver injury markers (ALT, AST, TBA, DBIL) and histopathological damage in a dose- and time-dependent manner.
TGE induced oxidative stress (decreased SOD/GSH/GSH-Px, increased MDA) and upregulated pro-inflammatory cytokines (IL-4, IL-1β).
Expression of the bile acid receptor FXR and transporters (BSEP, MRP2) was significantly downregulated.

Conclusions:

TGE induces cholestatic liver injury through a pathway involving oxidative stress, inflammation, and suppression of the FXR/BSEP/MRP2 axis.
The liver-on-a-chip model effectively simulates TGE-induced hepatotoxicity.
Further development with humanized systems is recommended for enhanced clinical relevance.