2. Academic Validation
  3. Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice

Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice

  • World J Hepatol. 2025 Mar 27;17(3):104520. doi: 10.4254/wjh.v17.i3.104520.
Jia-Lin Shi 1,  Tian Sun 1 2 3 4,  Qing Li 1 2 3 4,  Chun-Mei Li 1 2 3 4,  Jun-Fei Jin 1 2 3 4,  Chong Zhang 1 2 3 5
Affiliations

Affiliations

  • 1 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.
  • 2 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.
  • 3 China-USA Lipids in Health and Disease Research Center, Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China.
  • 4 Laboratory of Hepatobiliary and Pancreatic Surgery, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China.
  • 5 Laboratory of Hepatobiliary and Pancreatic Surgery, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China. chongzhang.1003@glmc.edu.cn.
PMID: 40177205 DOI: 10.4254/wjh.v17.i3.104520
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; C-jun-N-terminal kinase; Liver injury; Mogroside V; Reactive oxygen species.

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