Basic Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Mar 27, 2025; 17(3): 104520
Published online Mar 27, 2025. doi: 10.4254/wjh.v17.i3.104520
Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice
Jia-Lin Shi, Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang
Jia-Lin Shi, Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang, Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China
Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang, Guangxi Health Commission Key Laboratory of Basic Research in Sphingolipid Metabolism Related Diseases, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China
Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang, China-USA Lipids in Health and Disease Research Center, Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China
Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang, Laboratory of Hepatobiliary and Pancreatic Surgery, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China
Co-first authors: Jia-Lin Shi and Tian Sun.
Author contributions: Zhang C and Jin JF supervised the project and provided the fund support; Shi JL, Sun T, Li Q and Li CM performed the experiments; Shi JL, Sun T and Li Q analyzed the data; Zhang C wrote the manuscript with editing input from all authors. Shi JL and Sun T contributed equally to this work, so they are qualified to be joint first authors.
Supported by Guangxi Natural Science Foundation of China, No. 2024GXNSFAA010040; Special Fund of the Central Government Guiding Local Scientific and Technological Development by Guangxi Science and Technology Department, No. GuikeZY21195024; and National Natural Science Foundation of China, No. 82260499 and No. 82460463.
Institutional review board statement: This article does not pertain to human samples or clinical trials; therefore, no approval forms are necessary.
Institutional animal care and use committee statement: The study was reviewed and approved by the institutional animal care guidelines approved by the Experimental Animal Ethical Committee of Guilin Medical University (Approval No. GLMC-IACUC-20241084).
Conflict-of-interest statement: All the authors declare that they have no conflict of interest to disclose.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: No additional data are available.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chong Zhang, Associate Professor, Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, the Affiliated Hospital of Guilin Medical University, No. 15 Lequn Road, Guilin 541001, Guangxi Zhuang Autonomous Region, China. chongzhang.1003@glmc.edu.cn
Received: December 24, 2024
Revised: February 24, 2025
Accepted: March 6, 2025
Published online: March 27, 2025
Processing time: 92 Days and 16.2 Hours
Abstract
BACKGROUND

High levels of acetaminophen (APAP) consumption can result in significant liver toxicity. Mogroside V (MV) is a bioactive, plant-derived triterpenoid known for its various pharmacological activities. However, the impact of MV on acute liver injury (ALI) is unknown.

AIM

To investigate the hepatoprotective potential of MV against liver damage caused by APAP and to examine the underlying mechanisms.

METHODS

Mice were divided into three groups: Saline, APAP and APAP + MV. MV (10 mg/kg) was given intraperitoneally one hour before APAP (300 mg/kg) administration. Twenty-four hours after APAP exposure, serum transaminase levels, liver necrotic area, inflammatory responses, nitrotyrosine accumulation, and c-jun-N-terminal kinase (JNK) activation were assessed. Additionally, we analyzed reactive oxygen species (ROS) levels, JNK activation, and cell death in alpha mouse liver 12 (AML12) cells.

RESULTS

MV pre-treatment in vivo led to a reduction in the rise of aspartate transaminase and alanine transaminase levels, mitigated liver damage, decreased nitrotyrosine accumulation, and blocked JNK phosphorylation resulting from APAP exposure, without affecting glutathione production. Similarly, MV diminished the APAP-induced increase in ROS, JNK phosphorylation, and cell death in vitro.

CONCLUSION

Our study suggests that MV treatment alleviates APAP-induced ALI by reducing ROS and JNK activation.

Keywords: Acetaminophen; Mogroside V; Reactive oxygen species; Liver injury; C-jun-N-terminal kinase

Core Tip: This study examines whether mogroside V (MV), a plant-derived triterpenoid, can mitigate acetaminophen (APAP)-induced acute liver injury (ALI). Both animal and cell experiments demonstrate that MV alleviates APAP-induced ALI by suppressing reactive oxygen species/c-jun-N-terminal kinase signaling independent of glutathione modulation. Our findings suggest that MV could serve as a potential prophylactic agent to prevent APAP-induced ALI.