Knockout Apo E Mice
Mostrando 1-12 de 40 artigos, teses e dissertações.
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1. Alanyl-glutamine attenuates 5-fluorouracil-induced intestinal mucositis in apolipoprotein E-deficient mice
Apolipoprotein E (APOE=gene, apoE=protein) is a known factor regulating the inflammatory response that may have regenerative effects during tissue recovery from injury. We investigated whether apoE deficiency reduces the healing effect of alanyl-glutamine (Ala-Gln) treatment, a recognized gut-trophic nutrient, during tissue recovery after 5-FU-induced int
Braz J Med Biol Res. Publicado em: 28/04/2015
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2. Avaliação do óleo de sacha kiruma (Plukenetia volubilis L.) no duodeno e fígado de camundongos C57BL/6 e APO E-/- / Evaluation of the effects of sacha kiruma oil (Plukenetia volubilis L.) in the duodenum and liver in C57BL/6 and APO E -/- mice
Sacha kiruma (Plukenetia volubilis L.) é uma planta oleaginosa nativa da Amazônia Peruana. O óleo extraído de suas sementes é muito rico em ácidos graxos poliinsaturados, diretamente relacionados à prevenção de doenças cardiovasculares, dentre elas, a aterosclerose. Para seu transporte, os lipídeos formam complexos com proteínas, as apoproteínas
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 16/09/2011
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3. Interaction of high fat diet, conjugated linoleic acid and exercise on lipoprotein metabolism in mice genetically modified for atherosclerosis / Interação da dieta hiperlipídica, do ácido linoleico conjugado e do exercício físico no metabolismo lipoproteico em camundongos geneticamente modificados para aterosclerose
A aterosclerose tem sido a causa principal de doenças coronarianas. Ela é causada pelo aumento das lipoproteínas (LDL, IDL, VLDL, e remanescentes de quilomícrons) no plasma e turbulências hemodinâmicas. Como conseqüência, ocorre uma disfunção endotelial, aumentando a permeabilidade da íntima às lipoproteínas plasmáticas favorecendo a retenção
Publicado em: 2009
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4. Evolução da lesão aterosclerótica e perfil lipídico de camundongos knockout Apo E alimentados com resíduo de café seco e fermentado / Evaluation of the atherosclerotic lesion and lipid profile of Apo E Knockout mice fed with dry residue of coffee and fermentaded
A cafeicultura é uma atividade agrícola que produz um grande volume de resíduos líquidos e sólidos, gerando custos com o tratamento e destinação dos mesmos. O resíduo do fruto do cafeeiro, por ser rico em macro e micro nutrientes como açúcares, proteínas, Ca, Mg, P, N e K, torna-se um meio indutor para o crescimento e cultivo de fungos. Os fungos
Publicado em: 2008
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5. Effect of Lactobacillus delbrueckii on cholesterol metabolism in germ-free mice and on atherogenesis in apolipoprotein E knock-out mice
Elevated blood cholesterol is an important risk factor associated with atherosclerosis and coronary heart disease. Several studies have reported a decrease in serum cholesterol during the consumption of large doses of fermented dairy products or lactobacillus strains. The proposed mechanism for this effect is the removal or assimilation of intestinal cholest
Brazilian Journal of Medical and Biological Research. Publicado em: 2006-05
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6. Atherogenic effect of air pollution: association to anti-oxLDL and anti peptide D- ApoB and imorphometric and inflamatory aspects / Efeito aterogênico da poluição atmosférica: associação aos anticorpos anti LDLox e anti peptídeo D da apoB e aos aspectos morfométricos e inflamatórios
A poluição atmosférica de grandes centros urbanos é relacionada com o aumento dos índices de mortalidade e morbidade, principalmente em indivíduos com predisposição às doenças cardiovasculares e progressão da aterosclerose. Com o objetivo de verificar o potencial aterogênico da poluição atmosférica da cidade de São Paulo avaliamos o comportam
Publicado em: 2006
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7. Apolipoprotein E regulates dietary cholesterol absorption and biliary cholesterol excretion: Studies in C57BL/6 apolipoprotein E knockout mice
The present study examined the role of apolipoprotein E (apoE) in the regulation of dietary cholesterol absorption and biliary cholesterol excretion. Increasing dietary cholesterol from 0.02% to 0.5% in C57BL/6 wild-type mice decreased the percentage of dietary cholesterol that is absorbed by 25%, and this decrease was associated with a 2-fold increase in ga
The National Academy of Sciences.
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8. Apolipoprotein AI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice.
Apolipoprotein E (apo E)-deficient mice are severely hypercholesterolemic and develop advanced atheromas independent of diet. The C57BL/6 strain differs from most inbred strains by having lower HDL concentrations and a high risk of developing early atherosclerotic lesions when fed an atherogenic diet. The relative HDL deficiency and atherosclerosis susceptib
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9. IFN-gamma potentiates atherosclerosis in ApoE knock-out mice.
The early colocalization of T cells and the potent immunostimulatory cytokine IFN-gamma to atherosclerotic lesions suggest that the immune system contributes to atherogenesis. Since mice with a targeted disruption of the apoE gene (apoE 0 mice) develop profound atherosclerosis, we examined the role of IFN-gamma in this process. First, the presence of CD4(+)
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10. Cholesterol lowering in low density lipoprotein receptor knockout mice overexpressing apolipoprotein E.
Apo E is a key molecule in the lipoprotein metabolism; thus, genetic manipulation of apo E may prove useful in the treatment of hypercholesterolemia. To test the feasibility of this idea, we have generated low density lipoprotein receptor (LDLR) knockout mice that overexpress the rat apo E transgene (ETg+/+:LDLRKO), and compared their plasma lipoprotein prof
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11. Substitution of the carboxyl-terminal domain of apo AI with apo AII sequences restores the potential of HDL to reduce the progression of atherosclerosis in apo E knockout mice.
HDL metabolism and atherosclerosis were studied in apo E knockout (KO) mice overexpressing human apo AI, a des- (190-243)-apo AI carboxyl-terminal deletion mutant of human apo AI or an apo AI-(1-189)-apo AII-(12-77) chimera in which the carboxyl-terminal domain of apo AI was substituted with the pair of helices of apo AII. HDL cholesterol levels ranked: apo
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12. Increased sphingomyelin content of plasma lipoproteins in apolipoprotein E knockout mice reflects combined production and catabolic defects and enhances reactivity with mammalian sphingomyelinase.
Apolipoprotein E knockout (apoE0) mice accumulate atherogenic remnant lipoproteins in plasma. We now provide evidence that these particles are enriched in sphingomyelin (SM), and explore the mechanisms and possible pathophysiological consequences of this finding. The phosphatidylcholine/sphingomyelin (PC/SM) ratio was reduced in all lipoproteins in apoE0 mic