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Abstract Title:

Experimental Study on 1,25(OH)2 D3 Amelioration of Oral Lichen Planus through Regulating NF-κB Signaling Pathway.

Abstract Source:

Oral Dis. 2017 Feb 23. Epub 2017 Feb 23. PMID: 28231625

Abstract Author(s):

Jie Du, Ran Li, Feiyan Yu, Fang Yang, Jinhua Wang, Qingyong Chen, Xiangyu Wang, Bin Zhao, Fang Zhang

Article Affiliation:

Jie Du

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&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 siRNA 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 D3 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-κB (NF-κB) inhibitor and by activator protein 1 (AP-1) inhibitor, VDR-dependent 1,25(OH)2 D3 blocked the activation of phosphorylated-NF-κB p65 rather than c-Jun/c-Fos in the presence of LPS stimulation.

CONCLUSION: These results suggest that 1,25(OH)2 D3 plays an anti-inflammatory role in OLP by mediating NF-κB 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. This article is protected by copyright. All rights reserved.

Study Type : Human In Vitro

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