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

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.