To investigate the effects of Melissa officinalis extract (MOE) on inflammatory signaling in oral epithelial cells, particularly its modulation of JAK/STAT pathways.
Approach:
Composition Analysis: MOE was characterized using HPLC-HRMS.
Biological Effect Assessment: Transcriptomic, RT-qPCR, ELISA, immunofluorescence, and cell-free kinase analyses were employed to define MOE's biological effects in HSC2 and non-transformed epithelial cells.
Key Findings:
MOE was cytocompatible and selectively attenuated interferon-associated signaling.
It reduced interferon-stimulated gene expression, including MX1/2, IFIT, OAS family members, STAT1/2, CXCL10, and GBP1.
NF-κB-dependent CXCL8 expression remained unaffected.
MOE reduced JAK2 activity and suppressed STAT1 phosphorylation-associated nuclear translocation.
Caffeic acid was identified as a phenolic acid that suppresses CXCL10 production.
Interpretation:
MOE acts as a pathway-selective modulator of interferon-driven inflammatory responses in oral epithelial cells.
Limitations:
The study does not explore the long-term effects of MOE on oral inflammatory diseases.
Further investigation is needed to fully understand the mechanisms of action of MOE.
Conclusion:
These findings support further investigation of Melissa officinalis-derived preparations for targeted modulation of mucosal inflammation.
