Increased visfatin expression is associated with nuclear factor-kappa B and phosphatidylinositol 3-kinase in periodontal inflammation
Clinical Oral Investigations, cilt.21, sa.4, ss.1113-1121, 2017 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 21 Sayı: 4
- Basım Tarihi: 2017
- Doi Numarası: 10.1007/s00784-016-1871-7
- Dergi Adı: Clinical Oral Investigations
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.1113-1121
- Anahtar Kelimeler: Nicotinamide phosphoribosyltransferase, Periodontitis, Nuclear factor-kappa B, Phosphatidylinositol 3-kinase, Apoptosis
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Objective: Visfatin is an adipocytokine that plays a role in regulating periodontal inflammation by as yet identified mechanisms. It has been suggested that visfatin mediates inflammation via activation of the nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3-kinase (PI3k) signaling pathways which play a role in the inhibition of neutrophil apoptosis. The aim of this study was to investigate the expression of visfatin, NF-κB (NF-κB1 and NF-κB2), PI3k, tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β) in the tissue of healthy individuals and patients with periodontitis. Materials and methods: Tissue biopsy samples were obtained from 21 patients with chronic periodontitis and from the gingiva of 19 healthy individuals undergoing crown lengthening. The mRNA expression levels of visfatin, NF-κB, PI3k, TNF-α, and IL-1β were evaluated by quantitative real-time PCR (qPCR). Also, visfatin protein expression was measured by immunohistochemistry. Results: Both qPCR and immunohistochemistry results revealed that the visfatin expression was higher in the tissues with periodontitis than in healthy tissues (P < 0.01). Similarly, the mRNA expression levels of NF-κB2, PI3k, and IL-1β were higher in tissues with periodontitis than in healthy gingival tissues (P < 0.01). Visfatin was positively correlated with the levels of NF-κB1 (r = 0.549, P < 0.05), NF-κB2 (r = 0.636, P < 0.05), PI3k (r = 0.682, P < 0.01), TNF-α (r = 0.558, P < 0.05), and IL-1β (r = 0.686, P < 0.01) in the tissues with periodontitis. Conclusions: Our results demonstrated that increased visfatin was associated with the expression of NF-κB and PI3k which may play a role in the pathogenesis of periodontitis. We suggest that increased visfatin may contribute to the inhibition of neutrophil apoptosis via the NF-κB and PI3k signaling pathways. Clinical relevance: Understanding the role of visfatin in periodontitis will enable the development of new treatment methods for inflammation.