PUBLICATION
Flavone C-Glycosides from Dianthus superbus L. Attenuate Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) via Multi-Pathway Regulations
- Authors
- Chu, M., Tong, Y., Zhang, L., Zhang, Y., Dang, J., Li, G.
- ID
- ZDB-PUB-250814-15
- Date
- 2025
- Source
- Nutrients 17: (Journal)
- Registered Authors
- Keywords
- Dianthus superbus L., MASLD, apoptosis, flavone C-glycosides, inflammation, insulin resistance, lipid metabolism
- MeSH Terms
-
- Animals
- Apoptosis/drug effects
- Disease Models, Animal
- Fatty Liver*/drug therapy
- Fatty Liver*/metabolism
- Flavones*/isolation & purification
- Flavones*/pharmacology
- Glycosides*/isolation & purification
- Glycosides*/pharmacology
- Humans
- Lipid Metabolism/drug effects
- Liver/drug effects
- Liver/metabolism
- Liver/pathology
- Molecular Docking Simulation
- Network Pharmacology
- PPAR gamma/metabolism
- Signal Transduction/drug effects
- Zebrafish
- PubMed
- 40806041 Full text @ Nutrients
Citation
Chu, M., Tong, Y., Zhang, L., Zhang, Y., Dang, J., Li, G. (2025) Flavone C-Glycosides from Dianthus superbus L. Attenuate Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) via Multi-Pathway Regulations. Nutrients. 17:.
Abstract
Background The metabolic dysfunction-associated steatotic liver disease (MASLD) represents an escalating global health concern, with effective treatments still lacking. Given its complex pathogenesis, multi-targeted strategies are highly desirable.
Methods This study reports the isolation of four flavone C-glycosides (FCGs) from Dianthus superbus L. and explores their potential in treating MASLD. The bioactivity and underlying mechanisms of FCGs were systematically evaluated by integrating network pharmacology, molecular docking, and zebrafish model validation.
Results Network pharmacology analysis revealed that FCGs may modulate multiple MASLD-related pathways, including lipid metabolism, insulin signaling, inflammation, and apoptosis. Molecular docking further confirmed strong binding affinities between FCGs and key protein targets involved in these pathways. In the zebrafish model of MASLD induced by egg yolk powder, FCGs administration markedly attenuated obesity, hepatic lipid accumulation, and liver tissue damage. Furthermore, FCGs improved lipid metabolism and restored locomotor function. Molecular analyses confirmed that FCGs upregulated PPARγ expression to promote lipid metabolism, restored insulin signaling by enhancing INSR, PI3K, and AKT expression, and suppressed inflammation by downregulating TNF, IL-6 and NF-κB. Additionally, FCGs inhibited hepatocyte apoptosis by elevating the BCL-2/BAX ratio.
Conclusions These findings highlight the multi-pathway regulatory effects of FCGs in MASLD, underscoring its potential as a novel therapeutic candidate for further preclinical development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping