Magnolol alleviates high-fat diet-induced steatosis, inflammation and fibrosis in obesity-associated liver injuries via MOGAT1-mediated lipid metabolism and NF-κB signaling
- 1Department of Gastroenterology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University
Abstract
Background: Magnolol (MAG), a bioactive compound from Magnolia officinalis, possesses anti-inflammatory and lipid-lowering properties, but its role in obesity-associated liver injury and its molecular targets remain unknown.
Methods: High-fat diet (HFD)-fed mice were treated with MAG (10 or 20 mg/kg) daily for 7 days. AML12 hepatocytes were challenged with PA with or without MAG pretreatment. Liver injury was evaluated by histology, serum biochemistry, qPCR and Western blot. RNA-seq and mechanistic studies were performed to identify MAG-regulated pathways and targets.
Results: MAG significantly reduced hepatic lipid accumulation, serum transaminases, and collagen deposition in HFD-fed mice. RNA-seq identified monoacylglycerol O-acyltransferase 1 (MOGAT1) as the most significantly downregulated lipogenic gene by MAG. MOGAT1 expression correlated positively with liver triglyceride and injury markers. MAG also suppressed HFD-induced NF-κB activation (reduced P65 phosphorylation and nuclear translocation, lower IL-6, TNF-α, IL-1β). These findings were recapitulated in PA-treated AML12 cells. Critically, MOGAT1 overexpression largely reversed MAG-mediated suppression of inflammatory and fibrotic responses, demonstrating a causal role of MOGAT1 in MAG’s protective effects.
Conclusion: MAG alleviates HFD-induced hepatic steatosis, inflammation and fibrogenic responses by suppressing MOGAT1-mediated triglyceride synthesis and subsequent NF-κB-driven inflammation. This study identifies MOGAT1 as a novel downstream effector and functional mediator of MAG, providing new mechanistic insight into its hepatoprotective action and supporting its therapeutic potential for obesity-associated liver injuries.
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BibTeX
@article{huang2026magnolol,
title = {{Magnolol alleviates high-fat diet-induced steatosis, inflammation and fibrosis in obesity-associated liver injuries via MOGAT1-mediated lipid metabolism and NF-κB signaling}},
author = {Ziqing Huang and Zixia Huang and Linfei Luo and Zhengqiang Wu and Zhili Wen and Zhihua Xiao},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1971993},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1971993/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Magnolol alleviates high-fat diet-induced steatosis, inflammation and fibrosis in obesity-associated liver injuries via MOGAT1-mediated lipid metabolism and NF-κB signaling
AU - Ziqing Huang
AU - Zixia Huang
AU - Linfei Luo
AU - Zhengqiang Wu
AU - Zhili Wen
AU - Zhihua Xiao
PY - 2026
DA - 2026/10/27
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1971993
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1971993/full
AB - Background: Magnolol (MAG), a bioactive compound from Magnolia officinalis, possesses anti-inflammatory and lipid-lowering properties, but its role in obesity-associated liver injury and its molecular targets remain unknown. Methods: High-fat diet (HFD)-fed mice were treated with MAG (10 or 20 mg/kg) daily for 7 days. AML12 hepatocytes were challenged with PA with or without MAG pretreatment. Liver injury was evaluated by histology, serum biochemistry, qPCR and Western blot. RNA-seq and mechanistic studies were performed to identify MAG-regulated pathways and targets. Results: MAG significantly reduced hepatic lipid accumulation, serum transaminases, and collagen deposition in HFD-fed mice. RNA-seq identified monoacylglycerol O-acyltransferase 1 (MOGAT1) as the most significantly downregulated lipogenic gene by MAG. MOGAT1 expression correlated positively with liver triglyceride and injury markers. MAG also suppressed HFD-induced NF-κB activation (reduced P65 phosphorylation and nuclear translocation, lower IL-6, TNF-α, IL-1β). These findings were recapitulated in PA-treated AML12 cells. Critically, MOGAT1 overexpression largely reversed MAG-mediated suppression of inflammatory and fibrotic responses, demonstrating a causal role of MOGAT1 in MAG’s protective effects. Conclusion: MAG alleviates HFD-induced hepatic steatosis, inflammation and fibrogenic responses by suppressing MOGAT1-mediated triglyceride synthesis and subsequent NF-κB-driven inflammation. This study identifies MOGAT1 as a novel downstream effector and functional mediator of MAG, providing new mechanistic insight into its hepatoprotective action and supporting its therapeutic potential for obesity-associated liver injuries.
SN - 1663-9812
ER -