Abstract
Nobiletin, a biologically active substance in the skin of citrus fruits, has been reported to be an effective anti-inflammatory, anticancer, and antimicrobial agent. In this study, we aimed to examine the anti-inflammatory effects of nobiletin on tumor necrosis factor- (TNF-) stimulated human periodontal ligament cells (HPDLCs). Our results demonstrated that nobiletin treatment could decrease the expressions of inflammatory cytokines (C-X-C motif chemokine ligand (CXCL)10, C-C motif chemokine ligand (CCL)2, and interleukin- (IL-) 8), matrix metalloproteinases (MMPs) (MMP1 and MMP3), and prostaglandin-endoperoxide synthase 2 (PTGS2) in TNF-stimulated HPDLCs. Moreover, we revealed that nobiletin could inhibit the activation of nuclear factor- (NF-) κB and protein kinase B (AKT1) pathways in TNF-stimulated HPDLCs. Furthermore, nobiletin treatment enhanced nuclear factor, erythroid 2 like 2 (NFE2L2) and heme oxygenase 1 (HMOX1) expressions in TNF-stimulated HPDLCs. In conclusion, these findings suggest that nobiletin can inhibit inflammatory responses in TNF-stimulated HPDLCs by inhibiting NF-κB and AKT1 activations and upregulating the NFE2L2 and HMOX1 expression.
Highlights
Pathogenic bacteria of periodontal disease could induce alveolar bone resorption in periodontal lesions
We previously reported that Tumor necrosis factor (TNF) could inhibit some kinds of chemokines and matrix metalloproteinase (MMP)s in human periodontal ligament cells (HPDLCs) [4,5,6]
It is important to find the bioactive substance that could inhibit the influence of TNF on HPDLCs because TNF is the main inducer of inflammation in periodontal lesions
Summary
Pathogenic bacteria of periodontal disease could induce alveolar bone resorption in periodontal lesions. Tumor necrosis factor (TNF) ( known as TNF-α) is positively involved in the pathogenesis of periodontal disease because it could induce chemokines, MMPs, and prostaglandin E2 (PGE2) production in periodontal resident cells including human periodontal ligament cells (HPDLCs) [1,2,3]. We previously reported that TNF could inhibit some kinds of chemokines and matrix metalloproteinase (MMP)s in HPDLCs [4,5,6]. Ransjö et al found that TNF treatment enhanced PGE2 production in HPDLCs [7]. It is important to find the bioactive substance that could inhibit the influence of TNF on HPDLCs because TNF is the main inducer of inflammation in periodontal lesions
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