罗汉果甜苷V通过减少小鼠体内的活性氧和c-Jun氨基末端激酶激活来预防对乙酰氨基酚诱导的肝损伤。
Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice.
作者信息
Shi Jia-Lin, Sun Tian, Li Qing, Li Chun-Mei, Jin Jun-Fei, Zhang Chong
机构信息
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.
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.
出版信息
World J Hepatol. 2025 Mar 27;17(3):104520. doi: 10.4254/wjh.v17.i3.104520.
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 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 .
CONCLUSION
Our study suggests that MV treatment alleviates APAP-induced ALI by reducing ROS and JNK activation.
背景
对乙酰氨基酚（APAP）的高剂量摄入可导致严重的肝毒性。罗汉果甜苷V（MV）是一种具有生物活性的植物源三萜类化合物，以其多种药理活性而闻名。然而，MV对急性肝损伤（ALI）的影响尚不清楚。
目的
研究MV对APAP所致肝损伤的肝保护潜力，并探讨其潜在机制。
方法
将小鼠分为三组：生理盐水组、APAP组和APAP+MV组。在给予APAP（300mg/kg）前1小时腹腔注射MV（10mg/kg）。APAP暴露24小时后，评估血清转氨酶水平、肝坏死面积、炎症反应、硝基酪氨酸积累和c-jun氨基末端激酶（JNK）激活情况。此外，我们分析了α小鼠肝12（AML12）细胞中的活性氧（ROS）水平、JNK激活和细胞死亡情况。
结果
MV预处理可降低天冬氨酸转氨酶和丙氨酸转氨酶水平的升高，减轻肝损伤，减少硝基酪氨酸积累，并阻止APAP暴露引起的JNK磷酸化，且不影响谷胱甘肽的产生。同样，MV可减轻APAP诱导的ROS增加、JNK磷酸化和细胞死亡。
结论
我们的研究表明，MV治疗通过降低ROS和JNK激活来减轻APAP诱导的ALI。
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