Navegando por Palavras-chave "Sinvastatina"
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- ItemAcesso aberto (Open Access)Contribuição da metformina e sinvastatina para o entendimento da relação da resistência a insulina a inflamação(Universidade Federal de São Paulo (UNIFESP), 2006) Bulcão, Caroline [UNIFESP]; Ferreira, Sandra Roberta Gouvea [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
- ItemAcesso aberto (Open Access)Efeito da sinvastatina sobre a pressão arterial, metabolismo glicídico, metabolismo lipídico e função endotelial em ratos espontaneamente hipertensos tornados obesos(Universidade Federal de São Paulo (UNIFESP), 2018-01-18) Ferreira, Diego Faria Marques [UNIFESP]; Cesaretti, Mario Luis Ribeiro [UNIFESP]; http://lattes.cnpq.br/6026967513178490; http://lattes.cnpq.br/5770785379698382INTRODUCTION: Systemic arterial hypertension and obesity are associated with several comorbidities, such as diabetes and endothelial dysfunction. Simvastatin with its pleiotropic effects act on several systems (inflammation, release of vasodilation factors, among others) and show beneficial effects. OBJECTIVE: To evaluate the effects of simvastatin administration on glucose metabolism, lipid metabolism and vascular responsiveness in spontaneously hypertensive rats (SHR) made obese. METHODS: Spontaneous hipertensive rats male with 12 weeks of life were divided into 4 groups: control (SHR, n = 7), SHR + hyperlipidemic diet (SHR + HIPER, n = 5), SHR + simvastatin (n = 7) and group (SHR + HIPER + SINVA, n = 7). The hyperlipidic diet was administered from the weaning period and the dose of simvastatin was 10mg / kg / day, by gavage from the 13th to the 20th week. Body mass and caudal blood pressure were evaluated weekly. At the end of the study, the oral glucose tolerance test (TTGO), insulin tolerance test (TTI), lipid dosage, determination of vascular reactivity and left ventricular mass and epididymal fat were performed. RESULTS: The induction of obesity did not alter the parameters related to tail blood pressure and body weight, even when associated with simvastatin. As for glucose metabolism the administration of a hyperlipidic diet resulted in a significant increase of the area under the glucose curve. The vascular reactivity to acetylcholine, the SHR + SINVA group showed improvement in vasodilatation, whereas the other groups, when the hyperlipidic diet was associated, their effects were abolished. In the dosage of triglycerides, the groups treated with simvastatin obtained a significant reduction in their values, as well as in total cholesterol (TC), low density lipoprotein (LDL) dosage, very low density lipoprotein (VLDL). Regarding the dosage of high density lipoprotein (HDL), the association of pharmacological treatment together with the induction of obesity caused a significant increase in their values. The hyperlipidic diet caused the groups to have a significant increase in the weight of epididymal fat. CONCLUSION: Simvastatin treatment was effective in determining improvement in the endothelial function of SHR rats, but not in SHR + HIPER + SINVA. The increase of the epididymal fat induced by the hyperlipidic diet despite the improvement of the parameters of lipid metabolism, prevented the benefits induced by simvastatin on endothelial function.
- ItemSomente MetadadadosEfeitos hipolipemiantes e pleiotropicos da sinvastatina e ezetimiba em individuos prediabeticos(Universidade Federal de São Paulo (UNIFESP), 2008) Kater, Ana Lucia de Almeida [UNIFESP]Efeitos hipolipemiantes e pleiotropicos da sinvastatina e ezetimiba em individuos pre-diabeticos. ALA Kater. Tese de doutorado. Universidade Federal de São Paulo, Escola Paulista de Medicina. São Paulo, 2008. As estatinas sao medicamentos consagrados na prevencao primaria e secundaria de eventos cardiovasculares. Este beneficio e atribuido ao seu efeito hipolipemiante e possivelmente a efeitos complementares denominados pleiotropicos. Dentre estes, destaca-se o efeito anti-inflamatorio, alem de outros sobre a funcao endotelial e coagulabilidade. Seus efeitos sobre a sensibilidade a insulina foram menos explorados e os resultados sao controversos. A ezetimiba, farmaco redutor da absorcao intestinal de colesterol e de fitoesterois, mostrou-se eficaz na diminuicao das concentracoes de LDL-c em monoterapia. Porem, sua utilidade mais estabelecida foi na combinacao com as estatinas, potencializando a queda da LDL-c. Aventa-se um efeito anti-inflamatorio aditivo com a combinacao destes medicamentos, mas nao se sabe se a combinacao teria maior beneficio sobre a resistencia a insulina e funcao endotelial. O presente ensaio clinico aleatorizado avaliou os efeitos da sinvastatina e ezetimiba, isoladamente ou em associacao, sobre o perfil lipidico, sensibilidade a insulina e sobre os estados pro-inflamatorio e pro-trombotico de pacientes prediabeticos. Foram rastreados 290 individuos e 56 pacientes preencheram todos os criterios de elegibilidade ate o fechamento do periodo de inclusao (1º de novembro de 2006). Ocorreram 6 desistencias de modo que 50 pacientes completaram pelo menos uma das etapas do protocolo (periodo ezetimiba, sinvastatina e periodo de combinacao medicamentosa), cada uma com duracao de 12 semanas. Em maio de 2007, encerrou-se a coleta de dados. O sorteio para o grupo de monoterapia inicial (ezetimiba e sinvastatina) garantiu adequada comparabilidade. A monoterapia com ezetimiba, mas nao com sinvastatina, reduziu medidas de adiposidade corporal. Conforme esperado, ambos os medicamentos provocaram quedas significantes nos niveis de colesterol total, LDL-c e apolipoproteina B, que foram mais marcantes com a combinacao dos mesmos. As concentracoes de proteina C reativa (PCR) diminuiram com a combinacao dos medicamentos (p<0,05), mas nao com as monoterapias. Os valores medios de excrecao urinaria de albumina (EUA) e plasminogen activator inhibitor-1 (PAI-1) cairam e foram significantemente menores apos o uso de sinvastatina quando comparado ao periodo pos- ezetimiba, alem de serem observados menores niveis de EUA com a combinacao no grupo que iniciou tratamento com sinvastastina. O acrescimo de sinvastatina a monoterapia com ezetimiba provocou diminuicao significante nos niveis circulantes de selectina-E e intravascular cellular adhesion molecule-1 (ICAM-1). Porem, as medias dos valores de glicose, insulina, adiponectina, HOMAIR, area sob a curva de insulina, demais marcadores inflamatorios (contagem de leucocitos, IL-6, TNF-α) nao se alteraram quer com as monoterapias, quer com a combinacao medicamentosa. Nossos achados apontam para um efeito anti-inflamatorio sinergico da combinacao dos medicamentos, refletido pela reducao da PCR, que pode representar beneficio adicional a acao hipolipemiante no que diz respeito a protecao cardiovascular. Tambem ha indicios, por este estudo, de que a sinvastatina possa ter outro efeito pleiotropico, o de impedir a deterioracao da funcao endotelial, refletido pela diminuicao das moleculas de adesao celular (selectina-E e ICAM-1) e pelos menores niveis de albuminuria e PAI-1 encontrados com o uso deste medicamento. Estudos prospectivos maiores, em outros estratos populacionais e de mais longa duracao deverao investigar se, de fato, a combinacao medicamentosa podera melhorar o prognostico cardiovascular, em parte decorrente de provaveis efeitos pleiotropicos
- ItemAcesso aberto (Open Access)Estudo do efeito da sinvastatina na expressão gênica dos PPARs α e γ e na expressão e secreção de leptina em adipócitos 3T3-L1 submetidos a estímulo inflamatório(Universidade Federal de São Paulo (UNIFESP), 2016-10-31) Kuniyoshi, Mariana [UNIFESP]; Batista, Marcelo Costa [UNIFESP]; http://lattes.cnpq.br/0614350233628814; http://lattes.cnpq.br/9244426986498757; Universidade Federal de São Paulo (UNIFESP)Visceral obesity is considered important in the development of Metabolic Syndrome (MS), and as pathophysiological basis related to epidemic incidence of cardiovascular events. The excessive expansion of adipose tissue mass resulting in hypertrophic adipocytes can be attributed as a significant cause for inflammation development. The increase in secretion of biologically active molecules such as leptin, a pro-inflammatory adipokines, results in a significant impact on the progression of the MS. The administration of drugs, used primarily for the treatment of dyslipidemia in pleiotropic actions and antiatherogenic has been a major focus of recent studies approaching inflammation as a strategy for reducing cardiovascular risk. Thus, the objective of this study was to investigate the effect of simvastatin on the leptin secretion and expression in mature adipocytes derived from 3T3-L1 cell line, at baseline and after stimulation with TNF- α, mimicking the inflammatory state of the MS. In addition, we analyzed the potential effects of simvastatin on reversal of the inflammatory response in 3T3-L1 adipocytes and possible involvement of receptors activated by peroxisome proliferators-alpha (PPAR-α) and gamma (PPAR-γ) in such conditions. Our results consolidate the concept of MS as an inflammatory disease caused by increased production of mediators of proinflammatory proteins, specifically leptin, in adipocitary cell models. We have also demonstrated that there was reduced expression of PPAR-α and PPAR-γ receptors, when subject to inflammatory stimulus. By contrast, we observed an increase in expression of these receptors in cells pre-treated with simvastatin and exposed to TNF-α stimulus. From the analysis of our results, we support, at the cellular level, the integral inflammatory state of obesity¬related to MS. We also demonstrated the beneficial effect of simvastatin in attenuating the inflammatory response associated with increased TNF-α and a possible relationship of the PPARs in the modulation of this response.