Publication: Anti-Fibrotic Effect of Oleamide Identified from the Moringa oleifera Lam. Leaves via Inhibition of TGF-β1-Induced SMAD2/3 Signaling Pathway
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Issued Date
2025-04-01
Resource Type
ISSN
16616596
eISSN
14220067
Scopus ID
2-s2.0-105002294916
Pubmed ID
40244247
Journal Title
International Journal of Molecular Sciences
Volume
26
Issue
7
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences Vol.26 No.7 (2025)
Suggested Citation
Khongpiroon C., Buakaew W., Brindley P.J., Potikanond S., Daowtak K., Thongsri Y., Potup P., Usuwanthim K. Anti-Fibrotic Effect of Oleamide Identified from the Moringa oleifera Lam. Leaves via Inhibition of TGF-β1-Induced SMAD2/3 Signaling Pathway. International Journal of Molecular Sciences Vol.26 No.7 (2025). doi:10.3390/ijms26073388 Retrieved from: https://hdl.handle.net/20.500.14740/20743
Corresponding Author(s)
Other Contributor(s)
Abstract
Moringa oleifera (MO) is a prominent plant in traditional medicine, widely recognized for its phytochemicals with anti-inflammatory properties. Liver fibrosis characterized by chronic inflammation and excessive extracellular matrix deposition may benefit from the therapeutic properties of MO. This report focuses on the potential of oleamide (OLA), a bioactive compound identified from MO, in mitigating liver fibrosis. The anti-fibrotic effects of OLA were evaluated by assessing the production of pro-inflammatory cytokines, gelatinase activity and the expression of genes and proteins associated with the TGF-β/SMAD2/3 pathway. The LX-2 human hepatic stellate cell line, in conjunction with TGF-β1, was employed to model fibrotic conditions. OLA treatment significantly reduced the production of pro-fibrotic effectors in the activated LX-2 cells. Molecular docking analysis demonstrated a high binding affinity of OLA to key proteins in the TGF-β/SMAD2/3 pathway, while qRT-PCR and Western blotting revealed that OLA suppressed the expression of COL1A1, COL4A1, SMAD2, SMAD3, SMAD4, MMP2, MMP9, ACTA2 and TIMP1. These findings indicate that OLA effectively attenuates the pro-inflammatory responses induced by TGF-β1 and inhibits the activation of LX-2 cells. Collectively, OLA holds significant potential as a therapeutic agent for the prevention and treatment of liver fibrosis via the modulation of the TGF-β/SMAD2/3 signaling pathway.