Sesamol As a Potential Anti‐Fibrotic Agent Targeting ECM Dynamics in Oral Submucous Fibrosis
). Cell viability was assessed using the MTT assay, and the anti-migration ability was examined through the scratch assay. Antifibrotic actions were also evaluated in Masson's trichrome staining (MTS), and quantification of fibrosis-related genes was performed to assess the results. Sesamol treatment suppressed OSMF cell viability in a dose-dependent manner, demonstrating cytotoxic and significant anti-proliferative effects. Scratch assay analysis showed sesamol demonstrated significant anti-migratory efficacy with delayed wound closure, whereas dexamethasone exerted an inhibitory effect. MTS showed that sesamol markedly reduced collagen buildup, highlighting its anti-fibrotic potential. Gene expression analysis showed that sesamol increased MMP-1 and MMP-2 while reducing COL1A2, α-SMA, and TGF-β1, promoting ECM degradation and suppression of fibrotic signaling. In contrast, dexamethasone modulated MMP expression and fibrosis-related genes. Dexamethasone, a standard clinically used corticosteroid for OSMF management, was used as the reference treatment to benchmark the molecular effects of sesamol. In conclusion, sesamol demonstrated a significant anti-proliferative, anti-migratory, and anti-fibrotic effect on primary OSMF fibroblasts, suggesting its potential to influence key profibrotic pathways. These findings highlight sesamol as a promising candidate for further preclinical studies in OSMF management.
Authors
- Shumaila Usman (ORCID: https://orcid.org/0000-0003-0506-5981)
- Talat Mirza (ORCID: https://orcid.org/0000-0001-6264-3966)
- Amreen Liaquat
- Samreen Ramzan
- Shahrukh Khan
- Anum Islam (ORCID: https://orcid.org/0009-0002-2879-4036)
Institutions
- Ziauddin University (PK)
Publication Details
- Journal
- Journal of Biochemical and Molecular Toxicology
- Published
- 2026-04-27
- DOI
- https://doi.org/10.1002/jbt.70863
- Primary Topic
- Oral Health Pathology and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00