ABSTRACT
OBJECTIVE: Brain stroke is the third most important cause of death in developed countries. We studied the effect of different dietary lipids on the outcome of a permanent ischemic stroke rat model. METHODS: Wistar rats were fed diets containing 7% commercial oils (S, soybean; O, olive; C, coconut; G, grape seed) for 35 d. Stroke was induced by permanent middle cerebral artery occlusion. Coronal slices from ischemic brains and sham-operated animals were supravitally stained. Penumbra and core volumes were calculated by image digitalization after 24, 48, and 72 h poststroke. Homogenates and mitochondrial fractions were prepared from different zones and analyzed by redox status, inflammatory markers, ceramide, and arachidonate content, phospholipase A2, NOS, and proteases. RESULTS: Soybean (S) and G diets were mainly prooxidative and proinflammatory by increasing the liberation of arachidonate and its transformation into prostaglandins. O was protective in terms of redox homeostatic balance, minor increases in lipid and protein damage, conservation of reduced glutathione, protective activation of NOS in penumbra, and net ratio of anti-to proinflammatory cytokines. Apoptosis (caspase-3, milli- and microcalpains) was less activated by O than by any other diet. CONCLUSION: Dietary lipids modulate NOS and PLA2 activities, ceramide production, and glutathione import into the mitochondrial matrix, finally determining the activation of the two main protease systems involved in programmed cell death. Olive oil appears to be a biological source for the isolation of protective agents that block the expansion of brain core at the expense of penumbral neurons.
Subject(s)
Antioxidants/therapeutic use , Brain/drug effects , Dietary Fats , Inflammation/prevention & control , Oxidative Stress/drug effects , Plant Oils/therapeutic use , Stroke , Animals , Antioxidants/pharmacology , Apoptosis , Biomarkers/metabolism , Brain/cytology , Brain/metabolism , Brain Ischemia/diet therapy , Brain Ischemia/metabolism , Brain Ischemia/pathology , Cocos , Diet , Dietary Fats/adverse effects , Dietary Fats/metabolism , Dietary Fats/pharmacology , Dietary Fats/therapeutic use , Inflammation/etiology , Inflammation/metabolism , Lipid Metabolism/drug effects , Male , Neurons , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Nitric Oxide Synthase/metabolism , Olea , Oxidation-Reduction , Plant Oils/adverse effects , Plant Oils/pharmacology , Rats, Wistar , Reactive Oxygen Species/adverse effects , Glycine max , Stroke/diet therapy , Stroke/etiology , Stroke/metabolism , Stroke/pathology , VitisABSTRACT
The brain has a central role in the regulation of energy stability of the organism. It is the organ with the highest energetic demands, the most susceptible to energy deficits, and is responsible for coordinating behavioral and physiological responses related to food foraging and intake. Dietary interventions have been shown to be a very effective means to extend lifespan and delay the appearance of age-related pathological conditions, notably those associated with brain functional decline. The present review focuses on the effects of these interventions on brain metabolism and cerebral redox state, and summarizes the current literature dealing with dietary interventions on brain pathology.
Subject(s)
Brain/metabolism , Caloric Restriction , Energy Metabolism , Aging , Alzheimer Disease/diet therapy , Amyotrophic Lateral Sclerosis/diet therapy , Animals , Arcuate Nucleus of Hypothalamus/physiology , Autophagy , Dietary Supplements , Epilepsy/diet therapy , Fatty Acids/metabolism , Feeding Behavior/physiology , Humans , Insulin Resistance , Longevity , Mitochondria/metabolism , Models, Biological , Nucleus Accumbens/physiology , Oxidation-Reduction , Paraventricular Hypothalamic Nucleus/physiology , Parkinson Disease/diet therapy , Signal Transduction , Sirtuin 1/physiology , Stroke/diet therapyABSTRACT
Fundamentos: Acidente vascular encefálico (AVE) é uma doença cerebrovascular frequente em adultos, e uma das maiores causas de morbimortalidade no mundo. Entreos principais fatores de risco para as doenças cardiocerebrovasculares está o consumo alimentar. Objetivo: Analisar o consumo alimentar, a inter-relaçãoentre macro e micronutrientes e seus riscos clínicos em pacientes pós-AVE.Métodos: Estudo de coorte transversal realizado nos ambulatórios de Otorrinolaringologia/Disfagia eNeurologia/Vascular, de hospital terciário, em pacientes com diagnóstico de AVE. A coleta de dados realizou-sede junho a agosto 2010. Inquérito dietético, recordatório 24 horas e anamnese foram utilizados para traçar oconsumo alimentar. Foram calculadas as necessidades nutricionais. Realizou-se análise estatística, adotando-sesignificância de 5%. Resultados: Amostra constituida por 38 pacientes com média de idade de 59,5 anos; destes, 34 pacientes eram hipertensos e 19 diabéticos. Verificou-se alto consumo de macronutrientes (carboidratos, lipídios e proteínas) e baixo consumo de micronutrientes (vitaminas, saisminerais). A presença da DM apresentou associação estatisticamente significativa pela análise de Mann-Whitney com a ingestão excessiva de calorias (p=0,006),carboidratos (p=0,006) e lipídios (p=0,029). Além disso, o diabetes foi confirmado como fator que favorece o AVE recorrente pela análise de regressão logística (p=0,025).Conclusão: Os pacientes pós-AVE apresentam hábitos alimentares inadequados, porém a limentação desbalanceada dessa população não se mostrou significativa como fator de risco para o aumento das chances da ocorrência de novos eventoscardiocerebrovasculares. No entanto, o DM isoladamente se mostrou como fator de risco para a recorrência de AVE.
Subject(s)
Humans , Male , Female , Middle Aged , Stroke/diet therapy , Stroke/mortality , Eating/standards , Diet , Risk Factors , Hypertension/complicationsABSTRACT
OBJETIVO: Avaliar o efeito da administração de uma dieta enteral industrializada com antioxidantes sobre as concentrações plasmáticas de tióis totais, carbonilas de proteínas e malondialdeído em pacientes após acidente vascular cerebral. MÉTODOS: A amostra foi constituída de 14 pacientes de um hospital geral que iniciaram nutrição enteral 48 horas após o evento. Falência múltipla, insuficiência hepática, obesidade mórbida e diabetes Mellitus associados foram critérios de exclusão. A dieta industrializada ofertada por gotejamento contínuo, com uso de bombas infusoras, continha mix de carotenoides, vitaminas C, E e minerais Se, Zn e Cu em sua formulação. As amostras de sangue foram coletadas antes do início da administração da dieta e após cinco dias de início da dieta enteral, somente de pacientes que tivessem recebido o volume necessário para completar o gasto energético total. Tióis plasmáticos e carbonilas de proteína foram determinados por meio do Reagente de Ellman e pela reação com dinitrofenilhidrazina respectivamente. O malondialdeído foi obtido pela determinação de substâncias reativas do ácido tiobarbitúrico. RESULTADOS: A média de idade foi M=70,3, DP=14,1 anos. Todos receberam acima de 100% da Dietary Reference Intakes para nutrientes antioxidantes, que não ultrapassaram os limites superiores toleráveis de ingestão. Não houve alteração da concentração de tióis, mas houve aumento da formação de carbonilas de proteínas (p=0,034). Nos pacientes entubados, esse marcador mostrou-se significativamente maior (p=0,048) após administração da dieta. Não houve diferença nas concentrações de malondialdeído após a oferta de antioxidantes dietéticos. CONCLUSÃO: A análise de biomarcadores não demonstrou redução do estresse oxidativo após administração de dieta enteral industrializada com antioxidantes.
OBJECTIVE: The aim of this study was to assess the effect of a commercial enteral diet with added antioxidants on total plasma thiol, protein carbonyl and malondialdehyde levels of stroke survivors. METHODS: Fourteen patients from a general hospital who had been started on enteral nutrition 48 hours after a stroke were included in the study. The exclusion criteria were multiple organ dysfunction syndrome, liver failure and morbid obesity associated with diabetes Mellitus. The commercial diet was fed by continuous drip via infusion pump and contained mixed carotenoids, vitamins C and E, and the minerals selenium, zinc and copper. Blood samples were collected at baseline and after 5 days of enteral diet, but only from patients whose diet intake met their total energy expenditure. Total plasma thiol and protein carbonyl levels were determined by Ellman's reagent and dinitrophenylhydrazine, respectively. Plasma malondialdehyde levels were measured by the assay of thiobarbituric acid reactive substances. RESULTS: The mean age of the sample was M=70.3 years, (SD=14.1). All patients received more than 100% of the Dietary Reference Intakes for the abovementioned antioxidants but none exceeded the tolerable upper limit. Plasma thiol and malondialdehyde levels did not vary over time but protein carbonyl levels were significantly higher (p=0.034), especially in intubated patients (p=0.048). CONCLUSION: Biomarker determinations showed that a commercial enteral diet with added antioxidants did not reduce oxidative stress.