Diabetes increases interleukin-17 levels in periapical, hepatic, and renal tissues in rats
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Data
2017-11-01
Autores
Azuma, Mariane Maffei [UNESP]
Gomes-Filho, João Eduardo [UNESP]
Prieto, Annelise Katrine Carrara [UNESP]
Samuel, Renata Oliveira [UNESP]
de Lima, Valéria Marçal Felix [UNESP]
Sumida, Dóris Hissako [UNESP]
Ervolino, Edilson [UNESP]
Cintra, Luciano Tavares Angelo [UNESP]
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Resumo
Objectives This study aimed to evaluate the association between endodontic infection and diabetes on interleukin-17 levels in periapical, hepatic, and renal tissues of rats. Design Forty male rats were divided into groups: normoglycemic rats (N), normoglycemic rats with apical periodontitis (N-AP), rats with experimental diabetes (ED), and rats with experimental diabetes and apical periodontitis (ED-AP). Diabetes was induced by intravenous streptozotocin injection, and blood sugar levels were monitored to confirm disease development. Apical periodontitis (AP) was induced by pulp exposure to the oral environment during 30 days. After 30 days, hepatic and renal tissues were obtained, and IL-17 levels were quantified by ELISA. The right hemi-jaw was used to quantify IL-17 levels by immunohistochemistry. The values obtained in parametric tests were tabulated and analyzed statistically by analysis of variance (ANOVA) and Tukey tests, and the values obtained for scores were statistically analyzed by using the Kruskal-Wallis and Dun tests. The level of significance was set at 5%. Results ED and ED-AP groups expressed significantly higher IL-17 levels in both hepatic and renal tissues (p < 0.05), compared to N and N-AP groups. Apical periodontitis (AP) in ED-AP group was significantly more severe than that in N-AP group (p < 0.05). Furthermore, there was a significantly larger increase in the IL-17 levels in ED-AP group compared to N group (p < 0.05). Conclusion Our results indicate that diabetes increases IL-17 levels in hepatic and renal tissues and also enhances IL-17 production in apical periodontitis area of rats.
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Apical periodontitis, Diabetes, Endodontic infection, Interleukin-17
Como citar
Archives of Oral Biology, v. 83, p. 230-235.