BACKGROUND: The aim of the present study was to evaluate the therapeutic efficacy of vasoactive intestinal peptide (VIP), an immunoregulatory molecule, in experimental periodontitis. METHODS: Sixty-three male Sprague-Dawley rats were divided into five groups: control; lipopolysaccharide (LPS); LPS + 0.1 nmol VIP; LPS + 1 nmol VIP; and LPS + 10 nmol VIP. Saline was injected into the gingiva of control rats on days 1, 3, and 5, whereas the other groups received injections of Escherichia coli LPS. VIP groups received intraperitoneal injections of relevant dosages on days 2, 4, 6, 8, and 10. The control and LPS groups were given saline instead of VIP in the same manner. On day 11, serum samples were obtained, and rats were sacrificed. Alveolar bone loss; serum levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, -10, and -18, soluble receptor activator of nuclear factor-kappa B ligand (sRANKL), and osteoprotegerin (OPG); and the immune expression of RANKL and OPG were evaluated. RESULTS: The application of VIP caused a dose-dependent decline in alveolar bone loss compared to the LPS group, but the differences were not significant (P >0.05). A reduction in the histologic findings of inflammation was observed in all VIP groups. The 1- and 10-nmol VIP groups showed significantly lower serum sRANKL and OPG levels compared to the LPS group (P <0.05). The number of positively stained vessels for endothelial OPG was greater in the 1-nmol VIP group than in the LPS group (P <0.05). CONCLUSION: When periodontitis was induced by E. coli LPS, VIP downregulated the inflammatory response and inhibited alveolar bone loss, possibly by differentially regulating the tissue levels of RANKL and OPG.
BACKGROUND: The aim of the present study was to evaluate the therapeutic efficacy of vasoactive intestinal peptide (VIP), an immunoregulatory molecule, in experimental periodontitis. METHODS: Sixty-three male Sprague-Dawley rats were divided into five groups: control; lipopolysaccharide (LPS); LPS + 0.1 nmol VIP; LPS + 1 nmol VIP; and LPS + 10 nmol VIP. Saline was injected into the gingiva of control rats on days 1, 3, and 5, whereas the other groups received injections of Escherichia coliLPS. VIP groups received intraperitoneal injections of relevant dosages on days 2, 4, 6, 8, and 10. The control and LPS groups were given saline instead of VIP in the same manner. On day 11, serum samples were obtained, and rats were sacrificed. Alveolar bone loss; serum levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, -10, and -18, soluble receptor activator of nuclear factor-kappa B ligand (sRANKL), and osteoprotegerin (OPG); and the immune expression of RANKL and OPG were evaluated. RESULTS: The application of VIP caused a dose-dependent decline in alveolar bone loss compared to the LPS group, but the differences were not significant (P >0.05). A reduction in the histologic findings of inflammation was observed in all VIP groups. The 1- and 10-nmol VIP groups showed significantly lower serum sRANKL and OPG levels compared to the LPS group (P <0.05). The number of positively stained vessels for endothelial OPG was greater in the 1-nmol VIP group than in the LPS group (P <0.05). CONCLUSION: When periodontitis was induced by E. coliLPS, VIP downregulated the inflammatory response and inhibited alveolar bone loss, possibly by differentially regulating the tissue levels of RANKL and OPG.
Authors: Cesar A Ossola; Pablo N Surkin; Antonela Pugnaloni; Claudia E Mohn; Juan C Elverdin; Javier Fernandez-Solari Journal: Inflamm Res Date: 2012-05-12 Impact factor: 4.575
Authors: Ran Cheng; Wen Liu; Rui Zhang; Yuchao Feng; Neil A Bhowmick; Tao Hu Journal: Front Cell Infect Microbiol Date: 2017-11-14 Impact factor: 5.293