Artigo
Experimental periodontal disease triggers coronary endothelial dysfunction in middle-aged rats: preventive effect of a prebiotic β-glucan
Carregando...
Notas
Data
Orientadores
Editores
Coorientadores
Membros de banca
Título da Revista
ISSN da Revista
Título de Volume
Editor
Oxford University Press (OUP)
Faculdade, Instituto ou Escola
Departamento
Programa de Pós-Graduação
Agência de fomento
Tipo de impacto
Áreas Temáticas da Extenção
Objetivos de Desenvolvimento Sustentável
Dados abertos
Resumo
Abstract
This study was aimed to verify the hypothesis that periodontal disease contributes to endothelial dysfunction in the coronary arteries of middle-aged rats. Besides we evaluated the effects of a prebiotic (β-glucan isolated from Saccharomyces cerevisiae) in preventing vascular dysfunction. The sample comprised young (sham and induced to periodontal disease) and middle-aged rats (sham, periodontal disease, sham-treated and periodontal disease-treated), at 12 and 57 weeks, respectively. The treated-groups received daily doses of β-glucan (50 mg/kg) orally (gavage) for 4 weeks, and periodontal disease was induced in the last 2 weeks by ligature. A myograph system assessed vascular reactivity. The expression of endothelial nitric oxide synthase (eNOS), cyclooxygenase 1 (COX-1), COX-2, p47phox, gp91phox, NF-KB p65, p53, p21, and p16 was quantified by western blotting. Serum hydroperoxide production was measured by the ferrous oxidation–xylenol orange (FOX-2) assay method. Interleukin-1 beta (IL-1β), IL-10, and tumor necrosis factor-alpha (TNF-α) levels were evaluated by spectroscopic ultraviolet-visible analysis. Periodontal disease in middle-aged rats was associated with reduced acetylcholine-induced relaxations of coronary artery rings affecting the endothelium-dependent hyperpolarization- and the nitric oxide-mediated relaxations. The endothelial dysfunction was related to eNOS downregulation, pronounced impairment of the EDH-mediated relaxation, increased IL-1β and TNF-α proinflammatory cytokines, and also upregulation of NADPH oxidase and COXs, starting accumulate aging markers such as p53/p21 and the p16. Treatment with β-glucan effectively reduced bone loss in periodontal disease and delayed endothelial dysfunction in the coronary artery. Our data show that yeast β-glucan ingestion prevented oxidative stress and synthesis of proinflammatory marker and prevented eNOS reduction induced by periodontal disease in middle-aged rats. These results suggest that β-glucan has a beneficial effect on the coronary vascular bed.
Descrição
Área de concentração
Agência de desenvolvimento
Palavra chave
Marca
Objetivo
Procedência
Impacto da pesquisa
Resumen
Palavras-chave
ISBN
DOI
Citação
SILVA, G. C. et al. Experimental periodontal disease triggers coronary endothelial dysfunction in middle-aged rats: preventive effect of a prebiotic β-glucan. Journals of Gerontology Series A-Biological Sciences and Medical Sciences, [S.l.], v. 76, n. 8, p. 1398-1406, Aug. 2021. DOI: 10.1093/gerona/glab066.
