4.7 Article

Bioaccessible (poly)phenol metabolites from raspberry protect neural cells from oxidative stress and attenuate microglia activation

期刊

FOOD CHEMISTRY
卷 215, 期 -, 页码 274-283

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.foodchem.2016.07.128

关键词

Polyphenols; Raspberry; Bioaccessibility; Oxidative stress; Neuroprotective mechanisms; Neuroinflammation

资金

  1. iNOVA4Health Research Unit [LISBOA-01-0145-FEDER-007344]
  2. Fundacao para a Ciencia e Tecnologia (FCT)/Ministerio da Ciencia e do Ensino Superior
  3. Fundo Europeu de Desenvolvimento Regional FEDER (Portugal)
  4. FCT [PTDC/SAU-FAR/118787/2010, UID/DTP/04138/2013, IF/01097/2013]
  5. EUBerry FP7 [KBBE-2010-4 265942]
  6. BacHBerry [FP7-KBBE-2013-613793]
  7. Scottish Government's Rural and Environment Science and Analytical Services Division
  8. [SFRH/BD/86584/2012]
  9. Fundação para a Ciência e a Tecnologia [SFRH/BD/86584/2012] Funding Source: FCT

向作者/读者索取更多资源

Neuroinflammation is an integral part of the neurodegeneration process inherent to several aging dysfunctions. Within the central nervous system, microglia are the effective immune cells, responsible for neuroinflammatory responses. In this study, raspberries were subjected to in vitro digestion simulation to obtain the components that result from the gastrointestinal (GI) conditions, which would be bioaccessible and available for blood uptake. Both the original raspberry extract and the gastrointestinal bioaccessible (GIB) fraction protected neuronal and microglia cells against H2O2-induced oxidative stress and lipopolysaccharide (LPS)-induced inflammation, at low concentrations. Furthermore, this neuroprotective capacity was independent of intracellular ROS scavenging mechanisms. We show for the first time that raspberry metabolites present in the GIB fraction significantly inhibited microglial pro-inflammatory activation by LPS, through the inhibition of Iba1 expression, TNF-alpha release and NO production. Altogether, this study reveals that raspberry polyphenols may present a dietary route to the retardation or amelioration of neurodegenerative-related dysfunctions. (C) 2016 Elsevier Ltd. All rights reserved.

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