Efeito e segurança de 6,7-dimetoxi-3-nitrocumarina (composto semissintético modificado a partir da 6,7-dimetoxicumarina obtida do caule de platymiscium floribundum vog) em um modelo de periodontite em ratas

Abstract

Periodontitis is an inflammation of the supporting tissues of the teeth with progressive loss of insertion and bone destruction as a result of the host's response to the presence of a dysbiotic microbiota. Thus, this study aimed to evaluate the anti-resorptive activity and safety of 6,7-dimethoxy-3-nitrocoumarin, modified from 6,7-dimethoxycoumarin obtained from the stem of Platymiscium floribundum in ligature-induced periodontitis in rats and the involvement of the HO-1 pathway in its mechanism of action. Periodontitis was induced by placing a sterile nylon (3.0) ligature around the left upper second molars. The rats received (oral gavage) once a day, for 11 days, 6,7-dimethoxy-3-nitrocoumarine (0.01, 0.1 or 1 mg / kg) or vehicle (0.9% saline solution + ethanol 0.1%). 6,7-dimethoxy-3-nitrocoumarin (0.1 or 1 mg / kg) reduced alveolar bone loss (1.88 ± 0.15; 1.05 ± 0.24, respectively), when compared to the group treated with vehicle (3.05 ± 0.30). 6,7-dimethoxy-3-nitrocoumarin (1 mg / kg) reduced levels of TNF-ɑ (2.33 ± 0.56) and IL-1β (19.87 ± 2.9) mRNA, while increasing HO-1 mRNA levels (43.40 ± 1.05) and catalase activity (46.42 ± 4.59), when compared to the vehicle-treated group (46.29 ± 8.43; 37.83 ± 4.38; 1.58 ± 0.11; 8.93 ± 1.86, respectively). There were no statistical differences (P> 0.05) in serum biochemical parameters (creatinine, TALP, ALT, AST) between groups. 6,7-dimethoxy-3-nitrocoumarin decreased inflammatory bone loss in ligature-induced periodontitis in rats and activation of the HO-1 pathway contributes at least partially to its protective effects