Experimental study on 1,25(<scp>OH</scp>)₂D₃ amelioration of oral lichen planus through regulating NF‐<i>κ</i>B signaling pathway

Abstract

Objective To explore the protective function of vitamin D ( VD )/vitamin D receptor ( VDR ) on the development of oral lichen planus ( OLP ) and elaborate the underling mechanism of it. Methods H&amp;E staining, myeloid peroxidase ( MPO ) assays, quantitative PCR ( qPCR ), Western blotting, and Elisa were used to test the human biopsies and serum. QPCR , Western blotting, Elisa, and si RNA transfection were also performed in LPS ‐induced keratinocytes to observe the functions of vitamin D and VDR . Results The lack of VDR in the diseased biopsies from OLP patients was associated with activated helper T‐cell type 1 (Th1)‐driven inflammatory response. Importantly, the status of serum 25‐hydroxyvitamin D of OLP patients was reduced consistently. In a cultured cell model, 1,25( OH ) 2 D 3 could downregulate excessive production of pro‐inflammatory factors induced by lipopolysaccharide ( LPS ) in keratinocyte HaCat cells. Mechanistically, even though LPS ‐induced cytokines in keratinocytes were inhibited both by nuclear factor‐ κ B ( NF ‐ κ B) inhibitor and by activator protein 1 ( AP ‐1) inhibitor, VDR ‐dependent 1,25( OH ) 2 D 3 blocked the activation of phosphorylated‐ NF ‐ κ B p65 rather than c‐Jun/c‐Fos in the presence of LPS stimulation. Conclusion These results suggest that 1,25( OH ) 2 D 3 plays an anti‐inflammatory role in OLP by mediating NF ‐ κ B signaling pathway but not AP ‐1 signaling pathway with a VDR ‐dependent manner, predicting vitamin D supplement may be a potential strategy for the OLP management.