Experimental periodontal disease triggers coronary endothelial dysfunction in middle-aged rats: preventive effect of a prebiotic β-glucan.

This study 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 four weeks, and periodontal disease was induced in the last two weeks by ligature. A myograph system assessed vascular reactivity. The expression of eNOS, COX-1, COX-2, p47 phox, gp91phox, NFKB-p65, p53, p21, p16 was quantified by Western blotting. Serum hydroperoxide production was measured by the FOX-2 method. IL-1β, IL-10, and 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 (EDH)- and the nitric oxide (NO)-mediated relaxations. The endothelial dysfunction was related to eNOS downregulation, increased IL-1β, TNF-α pro-inflammatory cytokines and also upregulation of NADPH oxidase, and COXs, inducing cell cycle inhibitory pathways, including the 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, pro-inflammatory markers synthesis, 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.