Publication: Investigating the Antifibrotic Effects of β-Citronellol on a TGF-β1-Stimulated LX-2 Hepatic Stellate Cell Model
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Issued Date
2024-07-01
Resource Type
eISSN
2218273X
Scopus ID
2-s2.0-85199603613
Pubmed ID
39062514
Journal Title
Biomolecules
Volume
14
Issue
7
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomolecules Vol.14 No.7 (2024)
Suggested Citation
Buakaew W., Krobthong S., Yingchutrakul Y., Potup P., Thongsri Y., Daowtak K., Ferrante A., Usuwanthim K. Investigating the Antifibrotic Effects of β-Citronellol on a TGF-β1-Stimulated LX-2 Hepatic Stellate Cell Model. Biomolecules Vol.14 No.7 (2024). doi:10.3390/biom14070800 Retrieved from: https://hdl.handle.net/20.500.14740/20891
Corresponding Author(s)
Other Contributor(s)
Abstract
Liver fibrosis, a consequence of chronic liver damage or inflammation, is characterized by the excessive buildup of extracellular matrix components. This progressive condition significantly raises the risk of severe liver diseases like cirrhosis and hepatocellular carcinoma. The lack of approved therapeutics underscores the urgent need for novel anti-fibrotic drugs. Hepatic stellate cells (HSCs), key players in fibrogenesis, are promising targets for drug discovery. This study investigated the anti-fibrotic potential of Citrus hystrix DC. (KL) and its bioactive compound, β-citronellol (β-CIT), in a human HSC cell line (LX-2). Cells exposed to TGF-β1 to induce fibrogenesis were co-treated with crude KL extract and β-CIT. Gene expression was analyzed by real-time qRT-PCR to assess fibrosis-associated genes (ACTA2, COL1A1, TIMP1, SMAD2). The release of matrix metalloproteinase 9 (MMP-9) was measured by ELISA. Proteomic analysis and molecular docking identified potential signaling proteins and modeled protein–ligand interactions. The results showed that both crude KL extract and β-CIT suppressed HSC activation genes and MMP-9 levels. The MAPK signaling pathway emerged as a potential target of β-CIT. This study demonstrates the ability of KL extract and β-CIT to inhibit HSC activation during TGF-β1-induced fibrogenesis, suggesting a promising role of β-CIT in anti-hepatic fibrosis therapies.