epiglucan and Vascular-Diseases

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.

Topics: Animals; beta-Glucans; Coronary Vessels; Dietary Fiber; Disease Models, Animal; Endothelium, Vascular; NADPH Oxidases; Nitric Oxide Synthase Type III; Oxidative Stress; Periodontal Diseases; Prebiotics; Protective Agents; Rats; Reactive Oxygen Species; Treatment Outcome; Vascular Diseases; Vasodilation

Clinical evidence suggests that microangiopathy may be induced by fungal infection. The present study evaluated the toxic effect of (1-->3) beta-D glucan, a major component of fungal cell wall, on cultured transformed glomerular endothelial cells (TF-GEN). When TF-GEN were exposed to increasing concentrations of (1-->3) beta-D glucan (beta-DG; 115 to 430 pg/ml) for 1 to 3 hours, concentration- and time-dependent increases in hydroxyl radical production were demonstrated by electron paramagnetic resonance spectrometry using 5, 5-dimethyl-1-pyrrolyne-N-oxide as a spin trap agent. The amount of radicals induced by 230 or 430 pg/ml beta-DG was comparable to that induced by E. coli LPS (1 or 10 microg/ml). The beta-DG-induced free radical production was associated with a subsequent increase in LDH release from TF-GEN. When TF-GEN pretreated with U78517F (0.1 or 1.0 microM), a lipophilic antioxidant, were stimulated with LPS (1 or 10 microg/ml) or beta-DG (230 pg/ml) for 3 hours, free radical production by TF-GEN was significantly reduced in cells pretreated with the higher concentration of U78517F. Thus, fungal (1-->3) beta-D glucan induces glomerular endothelial injury by stimulating cellular free radical production. Such a mechanism may underlie microangiopathy in systemic fungal infections.

Topics: Animals; beta-Glucans; Candida albicans; Candidiasis; Cattle; Cell Wall; Chromans; Electron Spin Resonance Spectroscopy; Endothelium, Vascular; Free Radical Scavengers; Free Radicals; Glucans; Kidney Glomerulus; Piperazines; Vascular Diseases