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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Effects of melatonin on insulin signaling and inflammatory pathways of rats with apical periodontitis

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Author(s):
Tavares, B. S. [1] ; Tsosura, T. V. S. [1] ; Mattera, M. S. L. C. [1] ; Santelli, J. O. [1] ; Belardi, B. E. [1] ; Chiba, F. Y. [2] ; Cintra, L. T. A. [2] ; Silva, C. C. [2] ; Matsushita, D. H. [1]
Total Authors: 9
Affiliation:
[1] Sao Paulo State Univ UNESP, PPGMCF, Programa Posgrad Multicentr Ciencias Fisiol, Dept Basic Sci, SBFis, Aracatuba - Brazil
[2] Sao Paulo State Univ UNESP, Sch Dent, Dept Prevent & Restorat Dent, Aracatuba - Brazil
Total Affiliations: 2
Document type: Journal article
Source: International Endodontic Journal; JAN 2021.
Web of Science Citations: 0
Abstract

Aim To verify the effects of melatonin supplementation on insulin sensitivity, plasma concentrations of inflammatory cytokines, insulin signalling and inflammatory pathways in the soleus (SM) and extensor digitorum longus (EDL) muscles of rats with apical periodontitis (AP). Methodology Seventy-two Wistar rats were distributed into 4 groups: (a) control (C), (b) control supplemented with melatonin (M), (c) AP (AP), and (d) AP supplemented with melatonin (AP + M). AP was induced by pulp exposure of the maxillary and mandibular right first and second molars to the oral environment. After AP induction, oral supplementation with 5 mg kg(-1) melatonin (diluted in drinking water) for 60 days was initiated. At the end of the treatment, the following were analysed: (1) plasma concentrations of insulin and inflammatory cytokines (TNF-alpha, IL-6, IL-1 beta and IL-10) using ELISA kits; (2) glycaemia using enzymatic assay; (3) insulin resistance using homoeostasis model assessment of insulin resistance (HOMA-IR) index; and (4) phosphorylation status of pp185 tyrosine, Akt serine, IKK alpha/beta, and JNK in SM and EDL using Western blot. Analysis of variance of two or three factors was performed, followed by the Bonferroni test. P values AP promoted insulin resistance, significantly increased (P < 0.05) plasma concentrations of pro-inflammatory cytokines (TNF-alpha, IL-6, and IL-1 beta), significantly decreased (P < 0.05) the concentration of anti-inflammatory cytokine IL-10, impaired insulin signalling in SM, and increased IKK alpha/beta phosphorylation status in SM and EDL. Melatonin supplementation in rats with AP improved insulin sensitivity, significantly decreased (P < 0.05) TNF-alpha and IL-1 beta, significantly increased (P < 0.05) IL-10 plasma concentrations, and changed the insulin signalling in soleus muscle and IKK alpha/beta phosphorylation status in SM and EDL muscles. Conclusions Melatonin is a potent adjuvant treatment for improving apical periodontitis-associated changes in insulin sensitivity, insulin signalling and inflammatory pathways. In addition, the negative impact of AP on general health was also demonstrated. (AU)

FAPESP's process: 18/23346-3 - Effects of melatonin in the insulin signaling and inflammatory pathway of rats with apical periodontitis
Grantee:Bruna Soares Tavares
Support type: Scholarships in Brazil - Master
FAPESP's process: 19/12995-3 - Effects of melatonin in the insulin signaling and inflammatory pathway of rats with apical periodontitis
Grantee:Julia Ogata Santelli
Support type: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 19/18589-7 - Assessment of insulin sensitivity, plasma concentrations of inflammatory cytokines, lipid profile and insulin and inflammatory pathways in rats with apical periodontitis treated with melatonin.
Grantee:Doris Hissako Sumida
Support type: Regular Research Grants