Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Bases de datos
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Neurosci Lett ; 699: 199-205, 2019 04 23.
Artículo en Inglés | MEDLINE | ID: mdl-30753908

RESUMEN

Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer's and Parkinson's. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer's as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effectively cleared S100A9 in these mouse brain tissues during post-TBI recovery. By using sequential immunohistochemistry we have shown that S100A9 was produced by both neuronal and microglial cells. However, Aß peptide deposits characteristic for Alzheimer's disease were not detected in any post-TBI animals. On the first and third post-TBI days S100A9 was found to aggregate intracellularly into amyloid oligomers, similar to what was previously observed in human TBI tissues. Complementary, by using Rayleigh scatting, intrinsic fluorescence and atomic force microscopy we demonstrated that in vitro S100A9 self-assembles into amyloid oligomers within minutes. Its amyloid aggregation is highly dependent on changes of environmental conditions such as variation of calcium levels, pH, temperature and reduction/oxidation, which might be relevant to perturbation of cellular and tissues homeostasis under TBI. Present results demonstrate that S100A9 induction mechanisms in TBI are similar in mice and humans, emphasizing that S100A9 is an important marker of brain injury and therefore can be a potential therapeutic target.


Asunto(s)
Lesiones Traumáticas del Encéfalo/metabolismo , Encéfalo/metabolismo , Calgranulina B/metabolismo , Modelos Animales de Enfermedad , Placa Amiloide/metabolismo , Agregación Patológica de Proteínas/metabolismo , Animales , Masculino , Ratones , Microglía/metabolismo , Neuronas/metabolismo
2.
J Food Sci ; 77(10): C1084-9, 2012 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-22957943

RESUMEN

UNLABELLED: Extra virgin olive oil (EVOO) is recognized as one of the healthiest foods for its high content of antioxidants, which forestall and slow down radical formation. Free radical-initiated oxidation is considered one of the main causes of rancidity in fats and oils. As a consequence, reliable protocols for the investigation of oil oxidation based on selective, noninvasive, and fast methods are highly desirable. Here we report an experimental approach based on UV-Vis absorbance, steady-state fluorescence, and electron paramagnetic resonance (EPR) spectroscopy for studying oxidation processes induced by temperature for a period up to 35 d on Sicilian EVOO samples. We followed the decrease in ß-carotene content during incubation time and observed changes in polyphenols and tocopherols during the oxidation processes, focusing on the time scale of those changes. Using EPR spectroscopy, the free radical formation in different oil samples is reported, providing a fingerprint for both the antioxidant content and temporal features of the oxidation process at its early stage. PRACTICAL APPLICATION: We monitor ß-carotene and chlorophyll in an auto-oxidation process. A protocol based on spectroscopic measurements is presented and can be used for the quality control process of commercial olive oil.


Asunto(s)
Espectroscopía de Resonancia por Spin del Electrón/métodos , Oxidación-Reducción , Aceites de Plantas/química , Antioxidantes/análisis , Aceite de Oliva , Polifenoles/análisis , Temperatura , Tocoferoles/análisis , beta Caroteno/análisis
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA