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dc.creatorAguilar, E. C.-
dc.creatorLeonel, A. J.-
dc.creatorTeixeira, L. G.-
dc.creatorSilva, A. R.-
dc.creatorSilva, J. F.-
dc.creatorPelaez, J. M. N.-
dc.creatorCapettini, L. S. A.-
dc.creatorLemos, V. S.-
dc.creatorSantos, R. A. S.-
dc.creatorAlvarez-Leite, J. I.-
dc.date.accessioned2020-02-06T13:36:05Z-
dc.date.available2020-02-06T13:36:05Z-
dc.date.issued2014-06-
dc.identifier.citationAGUILAR, E. C. et al. Butyrate impairs atherogenesis by reducing plaque inflammation and vulnerability and decreasing NFκB activation. Nutrition, Metabolism and Cardiovascular Diseases, [S. l.], v. 24, n. 6, p. 606-613, June 2014.pt_BR
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S093947531400009X?via%3Dihub#!pt_BR
dc.identifier.urihttp://repositorio.ufla.br/jspui/handle/1/38917-
dc.description.abstractBackground & aims Butyrate is a four-carbon fatty acid that presents anti-inflammatory, anti-oxidative and apoptotic properties in colon and several cell lines. Because atherosclerosis has important oxidative and inflammatory components, butyrate could reduce oxidation and inflammation, impairing atherogenesis. We evaluated the effects of butyrate supplementation of butyrate on atherosclerosis and its mechanisms of action. Methods and results ApoE knockout mice were fed on chow diet or 1% butyrate-supplemented chow diet (Butyrate) for 10 weeks to assess atherosclerosis lesions area and inflammatory status. Macrophage and endothelial cells were also pretreated with butyrate (0.5 mM) for 2 h before oxLDL stimulation to study oxLDL uptake and pro and anti-inflammatory cytokine production. Butyrate reduced atherosclerosis in the aorta by 50%. In the aortic valve, butyrate reduced CCL2, VCAM1 and MMP2 productions in the lesion site, resulting in a lower migration of macrophage and increased collagen depositions in the lesion and plaque stability. When EA.hy926 cells were pretreated with butyrate, oxLDL uptake, CD36, VCAM1, CCL2 TNF, IL1β and IL6 productions were reduced, whereas IL10 production was increased. These effects were accompanied by a lower activation of NFκB due to a lower nuclear translocation of the p65 subunit. Conclusion Oral butyrate is able to slow the progression of atherosclerosis by reducing adhesion and migration of macrophages and increasing plaque stability. These actions are linked to the reduction of CD36 in macrophages and endothelial cells, decreased pro-inflammatory cytokines and lower activation of NFκB all of these data support a possible role for butyrate as an atheroprotective agent.pt_BR
dc.languageen_USpt_BR
dc.publisherElsevierpt_BR
dc.rightsrestrictAccesspt_BR
dc.sourceNutrition, Metabolism and Cardiovascular Diseasespt_BR
dc.subjectButyratept_BR
dc.subjectAtherosclerosispt_BR
dc.subjectMacrophagept_BR
dc.subjectFatty acidpt_BR
dc.subjectButiratopt_BR
dc.subjectAterosclerosept_BR
dc.subjectMacrófagopt_BR
dc.subjectÁcidos graxospt_BR
dc.titleButyrate impairs atherogenesis by reducing plaque inflammation and vulnerability and decreasing NFκB activationpt_BR
dc.typeArtigopt_BR
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