Navegando por Autor "Pereira, Renata Rebeca"

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Açai improves non-alcoholic fatty liver disease (NAFLD) induced by fructose.
(2018) Carvalho, Mayara Medeiros de Freitas; Reis, Larissa Lélis Teixeira; Lopes, Juliana Márcia Macedo; Lage, Nara Nunes; Guerra, Joyce Ferreira da Costa; Zago, Helena Porto; Bonomo, Larissa de Freitas; Pereira, Renata Rebeca; Lima, Wanderson Geraldo de; Silva, Marcelo Eustáquio; Pedrosa, Maria Lúcia
Introduction: the excessive consumption of fructose can cause liver damage, characteristic of non-alcoholic fatty liver disease (NAFLD) associated with changes in lipid metabolism and antioxidant defenses. Açai, the fruit of Euterpe oleracea Mart., has demonstrated numerous biological activities, including anti-inflammatory, antioxidant, and lipid metabolism modulating action. Objective: we evaluated the benefits of açai supplementation on liver damage caused by replacing starch with fructose in rats. Methods: thirty male Fischer rats were divided into two groups, the control group (C, 10 animals), which consumed a standard diet (AIN-93M), and the fructose (F, 20 animals) group, which consumed a diet containing 60% of fructose. After eight weeks, 10 animals from the fructose group received 2% of lyophilized açai, and were called the açai fructose group (FA). The animals were fed ad libitum with these diets for another ten weeks. Serum, hepatic and fecal lipid profile, antioxidant enzymes and carbonylated protein were assessed and histopathological characterization of the liver was performed. Results: açai promoted the reduction of ALT activity in relation to the fructose group (F), reduced alkaline phosphatase to a level similar to that of the control group (C) in relation to the fructose group (F), and reduced catalase activity. The fruit also increased the ratio of total/oxidized glutathione (GSH/GSSG) and reduced the degree of macrovesicular steatosis and the number of inflammatory cells. Conclusion: the replacement of starch by fructose during this period was effective in promoting NAFLD. Açai showed attenuating effects on some markers of hepatic steatosis and inflammation.
Detailed search for protein kinase(s) involved in plasma membrane H+-ATPase activity regulation of yeast cells.
(2015) Pereira, Renata Rebeca; Castanheira, Diogo Dias; Teixeira, Janaina Aparecida; Bouillet, Leoneide Érica Maduro; Ribeiro, Erica Milena de Castro; Trópia, Maria José Magalhães; Alvarez, Florencia; Correa, Lygia Fátima da Mata; Mota, Bruno Eduardo Fernandes; Conceição, Luís Eduardo Fernandes Rodrigues da; Castro, Ieso de Miranda; Brandão, Rogélio Lopes
This study displays a screening using yeast strains deficient in protein kinases known to exist in Saccharomyces cerevisiae. From 95 viable single mutants, 20 mutants appear to be affected in the glucose-induced extracellular acidification. The mutants that are unaffected in calcium signaling were tested for their sensitivity to hygromycin B. Furthermore, we verified whether the remaining mutants produced enzymes that are appropriately incorporated at plasma membrane. Finally, we measure the kinetic properties of the enzyme in purified plasma membranes from glucose-starved as well as glucose-fermenting cells. We confirmed the kinase Ptk2 involvement in H+−ATPase regulation (increase of affinity for ATP). However, the identification of the kinase(s) responsible for phosphorylation that leads to an increase in Vmax appears to be more complex. Complementary experiments were performed to check how those protein kinases could be related to the control of the plasma membrane H+−ATPase and/or the potential membrane. In summary, our results did not permit us to identify the protein kinase(s) involved in regulating the catalytic efficiency of the plasma membrane H+−ATPase. Therefore, our results indicate that the current regulatory model based on the phosphorylation of two different sites located in the C-terminus tail of the enzyme could be inappropriate.
Dietary açai attenuates hepatic steatosis via adiponectin-mediated effects on lipid metabolism in high-fat diet mice.
(2015) Guerra, Joyce Ferreira da Costa; Maciel, Poliane Silva; Abreu, Isabel Cristina Mallosto Emerich de; Pereira, Renata Rebeca; Silva, Maísa; Cardoso, Leandro de Morais; Sant'Ana, Helena Maria Pinheiro; Lima, Wanderson Geraldo de; Silva, Marcelo Eustáquio; Pedrosa, Maria Lúcia
Polyphenols, especially anthocyanins, have been considered promising for the prevention of nonalcoholic fatty liver disease (NAFLD). This study investigated whether açai (Euterpe oleracea Mart.), a source of anthocyanins and recognized as one of the new “superfruits”, could alleviate high-fat diet (HFD)-induced NAFLD in mice. In HFD mice, aqueous açai extract (AAE) administration (3 g/kg) for six weeks improved insulin resistance index and increased adiponectin mRNA expression in adipose tissue and serum levels. Furthermore, AAE decreased the total liver triacylglycerol content and attenuated HFD-induced hepatic steatosis. This reduced hepatic lipid content was associated with AAE-mediated up-regulation of genes involved in adiponectin signaling, including adiponectin receptor 2, PPAR-α, and its target gene, carnitine palmitoyltransferase. Thus, dietary açai can protect liver from steatosis through its enhancement of adiponectin levels, improvement of insulin sensitivity, and increase in PPAR-α-mediated fatty acid oxidation.
Different source of commercial vegetable oils may regulate metabolic, inflammatory and redox status in healthy rats.
(2020) Gomes, Sttefany Viana; Dias, Bruna Vidal; Pereira, Renata Rebeca; Lúcio, Karine de Pádua; Souza, Débora Maria Soares de; Silva, André Talvani Pedrosa da; Brandão, Geraldo Célio; Cosenza, Gustavo Pereira; Queiroz, Karina Barbosa de; Costa, Daniela Caldeira
Our goal was to carry out a comparative study to evaluate the metabolic and inflammatory effects and the redox status of commercial vegetable oils supplementation [linseed (LO), coconut (VCO), and sunflower (SO)] in metabolically healthy rats. The results found in this study showed that the LO group decreased the HOMA-IR and hepatic cholesterol, and increased the serum levels of IL-6. Supplementation with VCO increased glucose and HOMA-IR, cholesterol concentration and serum triacylglycerol (TAG). In this group, there was also an increase in TBARS. In the SO group there was a decrease in serum concentrations of cholesterol and TAG and an increase in hepatic concentration of these lipids. In addition, in the SO group there was a decrease in hepatic and sérum concentrations of IL-6 and hepatic levels of TNF, as well as a decrease in the GSH/GSSG ratio, suggesting changes in glutathione metabolism and inflammatory mediators.
Efects of açai on oxidative stress, ER stress, and infammationrelated parameters in mice with high fat diet-fed induced NAFLD.
(2019) Carvalho, Mayara Medeiros de Freitas; Lage, Nara Nunes; Paulino, Alice Helena de Souza; Pereira, Renata Rebeca; Almeida, Letícia Trindade; Silva, Tales Fernando da; Magalhães, Cíntia Lopes de Brito; Lima, Wanderson Geraldo de; Silva, Marcelo Eustáquio; Pedrosa, Maria Lúcia; Guerra, Joyce Ferreira da Costa
Non-alcoholic fatty liver disease (NAFLD), the most predominant liver disease worldwide, is a progressive condition that encompasses a spectrum of disorders ranging from steatosis to steatohepatitis, and, ultimately, cirrhosis and hepatocellular carcinoma. Although the underlying mechanism is complex and multifactorial, several intracellular events leading to its progression have been identified, including oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, and altered endoplasmic reticulum (ER) homeostasis. Phenolic compounds, such as those present in açai (Euterpe oleracea Mart.), are considered promising therapeutic agents due to their possible beneficial effects on the prevention and treatment of NAFLD. We tested in vitro effects of aqueous açai extract (AAE) in HepG2 cells and its influence on oxidative stress, endoplasmic reticulum stress, and inflammation in a murine model of high fat diet-induced NAFLD. In vitro AAE exhibited high antioxidant capacity, high potential to inhibit reactive oxygen species production, and no cytotoxicity. In vivo, AAE administration (3 g/kg) for six weeks attenuated liver damage (alanine aminotransferase levels), inflammatory process (number of inflammatory cells and serum TNFα), and oxidative stress, through the reduction of lipid peroxidation and carbonylation of proteins determined by OxyBlot and modulation of the antioxidant enzymes: glutathione reductase, SOD and catalase. No change was observed in collagen content indicating an absence of fibrosis, stress-related genes in RE, and protein expression of caspase-3, a marker of apoptosis. With these results, we provide evidence that açai exhibits hepatoprotective effects and may prevent the progression of liver damage related to NAFLD by targeting pathways involved in its progression.
Estratégia para a identificação de proteína(s) quinase(s) envolvida(s) na ativação da H+- ATPase de membrana plasmática de Saccharomyces cerevisiae.
(Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa e Pós Graduação, Universidade Federal de Ouro Preto., 2011) Pereira, Renata Rebeca; Brandão, Rogélio Lopes
A H+-ATPase de membrana plasmática de Saccharomyces cerevisiae é uma bomba de prótons que possui um papel importante na fisiologia deste microrganismo, uma vez que ativada é capaz de criar um gradiente eletroquímico que é essencial para a captação de nutrientes. A presença de glicose desencadeia modificações pós-traducionais que aumentam a atividade da H+-ATPase. Trabalhos realizados em nosso laboratório demonstraram que a ativação da enzima, induzida por glicose, está de alguma maneira ligada ao metabolismo de cálcio. No entanto, a identidade da(s) proteína quinase(s) que leva à ativação da enzima ainda não foi identificada. Neste trabalho, nós mostramos os resultados de uma triagem com as cepas de levedura que apresentam deleções únicas em genes que codificam para proteínas quinases existentes em Saccharomyces cerevisiae. Para isso, foi avaliada a variação do pH extracelular durante o crescimento celular, com adição de glicose, de leveduras apresentando deleções únicas em genes que codificam para proteínas quinases conhecidas. As células foram cultivadas em placas de 96 poços em YPD 2%, e cada cultura foi avaliada com o indicador ácido-base púrpura de bromocresol. Nossos resultados demonstraram que das 95 amostras analisadas, 53 foram incapazes de promover a acidificação durante o crescimento celular. Quando a ativação induzida por glicose foi medida por meio da determinação da acidificação extracelular, apenas 20 mutantes apresentaram uma clara redução na taxa de acidificação, quando comparados à linhagem selvagem. Para eliminar as quinases que poderiam estar indiretamente envolvidas na regulação da ATPase, a sinalização de cálcio foi medida e 14 mutantes apresentaram níveis de cálcio normais durante a sinalização induzida por glicose. Posteriormente, nós determinamos as propriedades cinéticas da enzima, em membranas plasmáticas purificadas, de mutantes com deleção em genes que codificam para 7 das 14 proteínas selecionadas como potenciais candidatas ao mecanismo de fosforilação da H+-ATPase, incluindo a cepa selvagem correspondente. No entanto, essa abordagem não permitiu esclarecer completamente a(s) identidade(s) da(s) proteína(s) quinase(s) que leva(m) à ativação da H+-ATPase de membrana plasmática de Saccharomyces cerevisiae.
High-fat diet increases mortality and intensifies immunometabolic changes in septic mice.
(2023) Gomes, Sttefany Viana; Dias, Bruna Vidal; Machado Júnior, Pedro Alves; Pereira, Renata Rebeca; Souza, Débora Maria Soares de; Breguez, Gustavo Silveira; Lima, Wanderson Geraldo de; Magalhães, Cíntia Lopes de Brito; Cangussú, Silvia Dantas; Silva, André Talvani Pedrosa da; Queiroz, Karina Barbosa de; Calsavara, Allan Jefferson Cruz; Costa, Daniela Caldeira
Immunometabolic changes in the liver and white adipose tissue caused by high-fat (HF) diet intake may worse metabolic adaptation and protection against pathogens in sepsis. We investigate the effect of chronic HF diet (15 weeks) on mortality and immunometabolic responses in female mice after sepsis induced by cecum ligation and perforation (CLP). At week 14, animals were divided into four groups: sham C diet, sepsis C diet (C-Sp), sham HF diet (HF-Sh) and sepsis HF diet (HF-Sp). The surviving animals were euthanized on the 7th day. The HF diet decreased survival rate (58.3% vs. 76.2% C-Sp group), increased serum cytokine storm (IL-6 [1.41 ×; vs. HF-Sh], IL-1β [1.37 ×; vs. C-Sp], TNF [1.34 ×; vs. C-Sp and 1.72 ×; vs. HF-Sh], IL-17 [1.44 ×; vs. HF-Sh], IL-10 [1.55 ×; vs. C-Sp and 1.41 ×; HF-Sh]), white adipose tissue inflammation (IL-6 [8.7 ×; vs. C-Sp and 2.4 ×; vs. HF-Sh], TNF [5 ×; vs. C-Sp and 1.7 ×; vs. HF-Sh], IL-17 [1.7 ×; vs. C-Sp], IL-10 [7.4 ×; vs. C-Sp and 1.3 ×; vs. HF-Sh]), and modulated lipid metabolism in septic mice. In the HF-Sp group liver's, we observed hepatomegaly, hydropic degeneration, necrosis, an increase in oxidative stress (reduction of CAT activity [−81.7%; vs. HF-Sh]; increase MDA levels [82.8%; vs. HF-Sh], and hepatic IL-6 [1.9 ×; vs. HF-Sh], and TNF [1.3 × %; vs. HF-Sh]) production. Furthermore, we found a decrease in the total number of inflammatory, mononuclear cells, and in the regenerative processes, and binucleated hepatocytes in a HF-Sp group livers. Our results suggested that the organism under metabolic stress of a HF diet during sepsis may worsen the inflammatory landscape and hepatocellular injury and may harm the liver regenerative process.
Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers.
(2014) Abreu, Isabel Cristina Mallosto Emerich de; Guerra, Joyce Ferreira da Costa; Pereira, Renata Rebeca; Silva, Maísa; Lima, Wanderson Geraldo de; Silva, Marcelo Eustáquio; Pedrosa, Maria Lúcia
Objetivo: Determinar se uma dieta hipercolesterolemiante induz esteatose hepatica, alterações na expressão de mRNA da NADPH oxidase e nas defesas antioxidantes. Materiais e métodos: Ratas Fischer foram divididas em dois grupos de oito animais de acordo com o tratamento recebido, controle (C) e hipercolesterolemico (H). Aquelas do grupo C foram alimentadas com dieta padrão (AIN-93M) e as do grupo H foram alimentadas com dieta hipercolesterolemiante (25% de óleo de soja e 1% de colesterol). As dietas foram oferecidas por oito semanas. Resultados: O grupo H apresentou acumulo de lipídios no fígado, aumento das atividades de ALT e AST e da concentração de colesterol no soro comparado ao grupo C. O marcador da peroxidacão lipídica (TBARS) e os níveis de mRNA das subunidades p47phox da NADPH-oxidase e p22phox foram aumentados no fígado de animais do grupo H, alem de alteração da atividade e expressão de enzimas antioxidantes. Conclusão: Os resultados mostram um aumento na expressão de subunidades da NADPH oxidase e alterações na atividade das enzimas antioxidantes na esteatose hepática induzida por dieta hipercolesterolemiante.
Lpx1p links glucose-induced calcium signaling and plasma membrane H+-ATPase activation in Saccharomyces cerevisiae cells.
(2017) Castanheira, Diogo Dias; Santana, Eduardo Perovano; Santos, Fernanda Godoy; Diniz, Raphael Hermano Santos; Oliveira, Fábio Faria; Pereira, Renata Rebeca; Trópia, Maria José Magalhães; Castro, Ieso de Miranda; Brandão, Rogélio Lopes
In yeast, as in other eukaryotes, calcium plays an essential role in signaling transduction to regulate different processes. Many pieces of evidence suggest that glucose-induced activation of plasma membrane H+-ATPase, essential for yeast physiology, is related to calcium signaling. Until now, it was not identified any protein that could be regulated by calcium in this context. Lpx1p, a serine-protease that is also involved in the glucose-induced activation of the plasma membrane H+-ATPase activation, could be a candidate to respond to intracellular calcium signaling involved in this process. In this work, and by using different approaches, we showed many pieces of evidence suggesting that the requirement of calcium signaling for activation of the plasma membrane H+-ATPase is due to its requirement for activation of Lpx1p. According to the current model, activation of Lpx1p would cause hydrolysis of an acetylated tubulin that keeps the plasma membrane H+-ATPase in an inactive state. Therefore, after its activation, Lpx1p would hydrolyze the acetylated tubulin making the plasma membrane H+-ATPase phosphorylation accessible for at least one protein kinase.