). 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.
Ramzan et al. (Mon,) studied this question.