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Updated: Mar 14, 2026

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
Published on: May 13, 2016
Corosolic acid protects hepatocytes against ethanol-induced damage by modulating mitogen-activated protein kinases
Xiaolan Guo1, Ruibing Cui1, Jianjian Zhao1
1Department of Hepatology and Gastroenterology, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan, Shandong 250012, People's Republic of China.
Abstract:
The reactive oxygen species(ROS)/mitogen-activated protein kinase (MAPK) destroyed autophagy and the reactive oxygen species/mitogen-activated protein kinase (MAPK) pathway are considered closely related to ethanol-induced hepatocellular injury. Previous work indicated that corosolic acid, the natural extracts of leaves of the banaba tree, Lagerstroemia speciosa L., could protect the liver against ethanol-induced damage, but the underlying mechanism is unclear. In the study we found that corosolic acid significantly inhibited ethanol-induced apoptosis, increased level of tumor necrosis factor-α(TNF-α) and reactive oxygen species accumulation in vitro. Corosolic acid inhibited ethanol-activated p38 and c-Jun N-terminal kinase MAPK signaling in BRL-3A and HepG2 cells as well as in experimental rats. Corosolic acid restored the ethanol-suppressed expression of autophagy-related genes, including beclin-1 and the ratio of microtubule-associated protein light chain 3II/I (LC3II/I) via AMP-activated protein kinase (AMPK) activation both in vitro and in vivo. In experimental rats, corosolic acid ameliorated the detrimental histopathological findings. Corosolic acid may protect the liver against ethanol-induced injury by modulation of MAPK signaling and autophagy activation. These findings suggested that corosolic acid might be a promising agent in treatment of alcoholic liver diseases.
Insights
Corosolic acid protects the liver from alcohol damage by reducing harmful reactive oxygen species (ROS) and activating autophagy. This natural compound may be a promising treatment for alcoholic liver diseases.
Area of Science:
- Hepatology
- Molecular Biology
- Pharmacology
Background:
- Ethanol-induced liver injury is linked to reactive oxygen species (ROS)/mitogen-activated protein kinase (MAPK) pathways.
- Corosolic acid from banaba tree leaves shows potential liver protection, but its mechanism is unclear.
Purpose of the Study:
- To investigate the protective mechanism of corosolic acid against ethanol-induced liver injury.
- To explore corosolic acid's effects on MAPK signaling, autophagy, and related pathways.
Main Methods:
- In vitro studies using BRL-3A and HepG2 cells, and in vivo studies using experimental rats.
- Assessed apoptosis, ROS accumulation, TNF-α levels, MAPK signaling (p38, JNK), autophagy markers (beclin-1, LC3II/I), and AMPK activation.
- Examined histopathological changes in rat livers.
Main Results:
- Corosolic acid inhibited ethanol-induced apoptosis, ROS accumulation, and TNF-α levels.
- It suppressed ethanol-activated p38 and c-Jun N-terminal kinase MAPK signaling.
- Corosolic acid restored ethanol-suppressed autophagy via AMPK activation and improved liver histopathology.
Conclusions:
- Corosolic acid protects the liver against ethanol-induced injury by modulating MAPK signaling and activating autophagy.
- Corosolic acid shows promise as a therapeutic agent for alcoholic liver diseases.
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