Navegando por Palavras-chave "Omega 3"
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- ItemAcesso aberto (Open Access)Administração de ômega 3 em culturas de células neuronais (NEURO 2a): estudo da via de diferenciação celular NOTCH(Universidade Federal de São Paulo, 2023-04-26) Reis, Henrique Nogueira [UNIFESP]; Silva, Cristiano Mendes da [UNIFESP]; Simabuco, Fernando Moreira [UNIFESP]; http://lattes.cnpq.br/6362783289622710; http://lattes.cnpq.br/7868915353525184; http://lattes.cnpq.br/8128803570757548; Universidade Federal de São Paulo (UNIFESP)O ômega 3 é uma família de ácidos graxos formados pelos ácidos graxos essenciais, entre eles estão o ácido alfa linolênico (ALA), ácido eicosapentaenoico (EPA) e o ácido docosahexaenóico (DHA). O DHA auxilia na neurogênese, sugerindo que ele possui a propriedade de modular a função hipocampal regulada pela neurogênese com a promoção da diferenciação celular de células tronco em células neuronais maduras. A ativação da sinalização de Notch induz a expressão de genes repressores da transcrição, como o Hes1 e Hes5, levando à repressão da expressão do gene proneural e à manutenção de células-tronco/progenitoras neurais. O acréscimo de DHA para a promoção do crescimento e diferenciação neuronal, inclusive de oligodentritos, sugere um aumento significante da expressão de Notch1 e Hes1. Este estudo teve por objetivo avaliar in vitro, a via de sinalização celular Notch em linhagem celular de neuroblastos (células Neuro-2a) tratada com ácidos graxos ômega 3, e consequentemente averiguar inter-relação destes fatores com a neurogênese. Os experimentos in vitro foram realizados em culturas derivadas de neuroblastos e tratadas com um composto de ômega 3, rico em DHA durante 36h na concentração de 50μM e 100μM (DHA). Os resultados da expressão proteica de HES5 não apresentaram diferneça significativa, já a expressão de NOTCH1 e MASH1 tiveram uma significante diferença, principalmente nos tratamentos do grupo inflamado com LPS e adicionado 50μM e 100μM (DHA) (p=0,001). A inativação da família NOTCH/HES e seus genes relacionados regulam positivamente a expressão de MASH1 e aumentam a neurogênese. Considera-se que as célular Neuro-2a tratadas com o composto de ômega 3 apresentaram a sinalização celular da via NOTCH, aumentando a expressão de MASH1 e suprimindo a expressão de HES5 quando estimuladas a um ambiente de inflamação e tratamento com o composto a uma concentração de 100 μM de DHA.
- ItemAcesso aberto (Open Access)Efeito da suplementação com ácidos graxos ômega 3 (ω-3) nas propriedades das células estromais mesenquimais da medula óssea(Universidade Federal de São Paulo (UNIFESP), 2018-12-20) Oliveira, Andreia Silva de [UNIFESP]; Borges, Fernanda Teixeira [UNIFESP]; Schor, Nestor [UNIFESP]; http://lattes.cnpq.br/8276708741672261; http://lattes.cnpq.br/4206613998602417; http://lattes.cnpq.br/4123390663752858; Universidade Federal de São Paulo (UNIFESP)Mesenchymal stromal cells (MSCs) are characterized by the ability to differentiate into mesoderm cells, multiplication to maintain their undifferentiated state and expression of surface markers such as CD90 and CD73, but not CD45, in addition to others. They have ability to target the injured site and present antiinflammatories, antioxidants and immunosuppressants effects. Donor characteristics may influence the characteristics and / or effects of MSCs. This study aimed to perform dietary supplementation with omega3 polyunsaturated fatty acids in the characteristics of mesenchymal stromal cells. Wistar rats were supplemented for 28 days with eicosatetraenoic acid (EPA) and docosahexaenoic acid (DHA) (2mg/kg body weight), as MSCs were harvested, cultured and analyzed in the 4th passage (MSCs3) and compared with animal cells not supplemented (MSCs). The capacity of selfrenewal, adipogenic and osteogenic differentiation, response to hypoxia and repairing effect in a unilateral ureteral obstruction (UUO) model were analyzed. Differences in morphology and in the differentiation capacity between MSCs and MSCs3 was not observed. The latter has small capacity for selfrenewal, but both showed the same apoptotic rates under hypoxic conditions. In severe chronic diseases induced by UUO, we observed that as MSCs3 aggravated an infiltration of immune cells in relation to obstructed kidneys. In the transplanted kidneys with MSCs3, there was greater expression of superoxide dismutase1, IL10, and less IL6 production. There was no significant fibrosis in the obstructed kidneys, but there were increased levels of TGFβ1 in the UUO group. It decreased in those transplanted with MSCs3, suggesting a longterm antifibrotic effect as observed in MSCs. Our results suggest that supplementation of omega3 donors may interfere with the characteristics and effects of MSCs and supplementation should be taken into account when using these cells for therapy.
- ItemAcesso aberto (Open Access)Suplementação com ácidos graxos poliinsaturados (ômega 3 - EPA e DHA) para o tratamento de pacientes com epilepsia refratária : revisão sistemática e metanálise(Universidade Federal de São Paulo (UNIFESP), 2017-06-29) Vasconcelos, Vivian Sarmento de [UNIFESP]; Torloni, Maria Regina [UNIFESP]; http://lattes.cnpq.br/5661395483781554; http://lattes.cnpq.br/6022583540773749; Universidade Federal de São Paulo (UNIFESP)Objectives: To assess the effectiveness and safety of omega-3 polyunsaturated fatty acids (PUFA) in the control of seizures in patients with refractory epilepsy. Methods: Cochrane systematic review. We searched the following eletronic databases, without language restrictions: Cochrane Epilepsy Group Specialised Register, CENTRAL, MEDLINE, EMBASE, SCOPUS, LILACS and clinical trials registers. We included all randomised and quasi-randomised studies using PUFAs (in association with convential treatment) versus conventional treatment or other treatments for patients of any age with drug-resistant epilepsy. The following outcomes were assessed: seizure freedom, seizure reduction, improvement in quality of life, adverse effects and changes in plasma lipid profile. Two independent review authors were involved in study selection, data extraction and quality assessment of the included trials. Results: The search retrieved 71 citations, 8 studies were selected for full-text reading and 3 studies fulfilled the selection criteria and were included in the review. Two placebo controlled trials involving adults were conducted in developed countries, while one placebo controlled trial involving children was conducted in a developing country (Egypt). The three studies recruited a total of 155 subjects (85 adults and 70 children); 78 (43 adults and 35 children) were randomised to PUFAs and 77 (42 adults and 35 children) to placebo. All participants were followed for up to 12 weeks. Seizure freedom was reported by only one study, with a high risk of bias, involving exclusively children. The relative risk (RR) for this outcome was significantly higher in the children receiving PUFA compared to the control group: RR 20.00, 95% confidence interval (CI) 2.84 to 140.99, 1 study, 70 children. Similarly, PUFA supplementation was associated with a significant difference in the proportion of children with at least 50% reduction in seizure frequency: RR 33.00 95% CI 4.77 to 228.15, 1 study with a high risk of bias, 70 children. However, this effect was not observed when the data from two studies with adults were pooled: RR 0.57, 95% CI 0.19 to 1.75, I² 0%, 2 studies, 78 participants, low-quality evidence. None of the studies assessed bleeding as a potential adverse effect. There were no significant differences between the PUFA and control groups in relation to gastrointestinal effects: RR 0.78, 95% CI 0.32 to 1.89, 2 studies, 85 participants, low-quality evidence. Supplementation with PUFA did not produce significant differences in mean frequency of seizures, quality of life or other side effects. Conclusions: In view of the limited number of studies and small sample sizes, there is not enough evidence to support the use of PUFA supplementation in patients with refractory epilepsy. More trials are needed to assess the benefits of PUFA supplementation in the treatment of drug resistant epilepsy.