Please use this identifier to cite or link to this item: http://repositorio.ufla.br/jspui/handle/1/31709
Title: Oral butyrate reduces oxidative stress in atherosclerotic lesion sites by a mechanism involving NADPH oxidase down-regulation in endothelial cells
Keywords: Butyrate
Atherosclerosis
Oxidative stress
Reactive oxygen species
Short chain fatty acids
Lipids
Butirato
Aterosclerose
Estresse oxidativo
Espécies que reagem ao oxigênio
Ácidos graxos de cadeia curta
Lipídios
Issue Date: Aug-2016
Publisher: Elsevier
Citation: AGUILAR, E. C. et al. Oral butyrate reduces oxidative stress in atherosclerotic lesion sites by a mechanism involving NADPH oxidase down-regulation in endothelial cells. The Journal of Nutritional Biochemistry, Stoneham, v. 34, p. 99-105, Aug. 2016.
Abstract: Butyrate is a 4-carbon fatty acid that has antiinflammatory and antioxidative properties. It has been demonstrated that butyrate is able to reduce atherosclerotic development in animal models by reducing inflammatory factors. However, the contribution of its antioxidative effects of butyrate on atherogenesis has not yet been studied. We investigated the influence of butyrate on oxidative status, reactive oxygen species (ROS) release and oxidative enzymes (NADPH oxidase and iNOS) in atherosclerotic lesions of ApoE−/− mice and in oxLDL-stimulated peritoneal macrophages and endothelial cells (EA.hy926). The lesion area in aorta was reduced while in the aortic valve, although lesion area was unaltered, superoxide production and protein nitrosylation were reduced in butyrate-supplemented mice. Peritoneal macrophages from the butyrate group presented a lower free radical release after zymosan stimulus. When endothelial cells were pretreated with butyrate before oxLDL stimulus, the CCL-2 and superoxide ion productions and NADPH oxidase subunit p22phox were reduced. In macrophage cultures, in addition to a reduction in ROS release, nitric oxide and iNOS expression were down-regulated. The data suggest that one mechanism related to the effect of butyrate on atherosclerotic development is the reduction of oxidative stress in the lesion site. The reduction of oxidative stress related to NADPH oxidase and iNOS expression levels associated to butyrate supplementation attenuates endothelium dysfunction and macrophage migration and activation in the lesion site.
URI: https://www.sciencedirect.com/science/article/pii/S0955286316300699?via%3Dihub#!
http://repositorio.ufla.br/jspui/handle/1/31709
Appears in Collections:DNU - Artigos publicados em periódicos

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