Low Power Laser Irradiation Inhibits Arecoline-induced Oral Submucous Fibrosis

Objectives: Oral submucous fibrosis (OSF) is a precancerous condition, which is characterized as a juxtraepithelial inflammatory reaction and progressive fibrosis in oral submucosa and deeper connective tissues. It has been reported that an alkaloid compound of areca nut, arecoline, is a major etiological factor in the development of OSF.

Low-power laser irradiation (LPLI) has been applied for treating wound-healing, inflammation, muscle tissue repair and preventing fibrosis. Our previous studies indicated that LPLI may suppress inflammatory response in human adipose-derived stem cells via cAMP signaling pathway. Therefore, we investigate the molecular pathologic mechanisms of arecoline-induced OSF and evaluate the effects of LPLI arecoline-induced OSF.
Methods: Arecoline stimulated human gingival fibroblasts (HGF) were treated with or without low power laser irradiation (LPLI). The expression of fibrotic marker genes, such as TGF-β, α-SMA and CTGF, were analyzed by real-time PCR and Western blots. And the transcriptional activity of CTGF was further determined by the reporter assay.
Results: Our preliminary data show that arecoline increased mRNA and protein expressions of TGF-β, α-SMA and CTGF in HGF. Interestingly, both LPLI and forskolin , an adenylyl cyclase activator, reduced the expressions of arecoline-mediated fibrotic marker genes and inhibited the transcription activity of CTGF. Moreover, pretreatment of SQ22536, an adenylyl cyclase inhibitor, blocked the LPLI’s inhibitory effect of the expressions of arecoline-mediated fibrotic marker genes.
Conclusions: Our data suggest that LPLI may have anti-fibrotic effects via the cAMP signaling pathway.