Abstract
Aim:
To verify the effects of melatonin supplementation on insulin sensitivity, plasma concentrations of inflammatory cytokines, insulin signaling 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 in 4 groups: a) control (C), b) control supplemented with melatonin (M), c) AP (AP), and d) AP supplemented with melatonin (AP + M). AP were induced by dental 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 melatonin (diluted in drinking water) for 60 days was initiated. At the end of the treatment, the following were analyzed: 1) plasma concentrations of insulin and inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-10) using ELISA kits; 2) glycemia using enzymatic assay; 3) insulin resistance using homeostasis model assessment of insulin resistance (HOMA-IR) index; 4) phosphorylation status of pp185 tyrosine, Akt serine, IKKα/β, 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 < 0.05 were considered statistically significant.
Results:
AP promoted insulin resistance, significantly increased (p < 0.05) plasma concentrations of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), significantly decreased (p < 0.05) the concentration of anti-inflammatory cytokine IL-10, impaired insulin signaling in SM, and increased IKKα/β phosphorylation status in SM and EDL. Melatonin supplementation in rats with AP improved insulin sensitivity, significantly decreased (p < 0.05) TNF-α and IL-1β, significantly increased (p < 0.05) IL-10 plasma concentrations, and changed the insulin signaling in soleus muscle and IKKα/β phosphorylation status in SM and EDL.
Conclusions:
Melatonin is a potent adjuvant treatment for improving apical periodontitis -associated changes in insulin sensitivity, insulin signaling and inflammatory pathways. In addition, the negative impact of AP on general health was also demonstrated.
Full text
