Osthole Induces Hepatic Stellate Cell Ferroptosis to Alleviate Liver Fibrosis by Inhibiting the Y-Box Binding Protein 1-Wnt/β-Catenin Axis Through Downregulating Myocyte Enhancer Factor 2A
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View abstract on PubMed
Summary
This summary is machine-generated.Osthole (OST) alleviates liver fibrosis by triggering ferroptosis in hepatic stellate cells (HSCs). It inhibits HSC activation via the MEF2A/YBX1/Wnt/β-catenin pathway, offering a potential therapeutic strategy.
Area Of Science
- Hepatology
- Cell Biology
- Pharmacology
Background
- Liver fibrosis is a significant health concern linked to ferroptosis.
- Osthole (OST) demonstrates therapeutic potential for liver fibrosis.
Purpose Of The Study
- To investigate OST's effects on ferroptosis in hepatic stellate cells (HSCs) during liver fibrosis.
- To elucidate the underlying molecular mechanisms of OST's action.
Main Methods
- Established a CCl4-induced mouse model of liver fibrosis.
- Utilized MTT and EDU assays for cell viability and proliferation.
- Performed dual luciferase reporter and ChIP assays to analyze protein interactions.
Main Results
- OST treatment alleviated liver fibrosis by inducing ferroptosis in HSCs.
- OST inhibited HSC activation in vitro, effects reversed by MEF2A or YBX1 overexpression.
- MEF2A activated Wnt/β-catenin signaling by upregulating YBX1 expression.
Conclusions
- OST mitigates liver fibrosis by promoting HSC ferroptosis and inhibiting activation.
- The mechanism involves the MEF2A/YBX1/Wnt/β-catenin signaling axis.
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