Abstract
Chronic neuroinflammation associated with neurodegenerative disorders has been reported to be prevented by dietary components. Particularly, dietary (poly)phenols have been identified as having anti-inflammatory and neuroprotective actions, and their ingestion is considered a major preventive factor for such disorders. To assess the relation between (poly)phenol classes and their bioactivity, we used five different raspberry genotypes, which were markedly different in their (poly)phenol profiles within a similar matrix. In addition, gastro-intestinal bio-accessible fractions were produced, which simulate the (poly)phenol metabolites that may be absorbed after digestion, and evaluated for anti-inflammatory potential using LPS-stimulated microglia. Interestingly, the fraction from genotype 2J19 enriched in ellagitannins, their degradation products and ellagic acid, attenuated pro-inflammatory markers and mediators CD40, NO, TNF-α, and intracellular superoxide via NF-κB, MAPK and NFAT pathways. Importantly, it also increased the release of the anti-inflammatory cytokine IL-10. These effects contrasted with fractions richer in anthocyanins, suggesting that ellagitannins and its derivatives are major anti-inflammatory (poly)phenols and promising compounds to alleviate neuroinflammation
Highlights
Microglia are the resident innate immune cells in the central nervous system (CNS)
Various studies have reported reduced microglial pro-inflammatory activation by inhibiting NFAT [47] or NF-kB [48], and here we demonstrated that 2J19phenol metabolites are capable of similar effects
A previous study has shown that ellagic acid (EA) inhibits human platelet activation upon stimulation with hydrogen peroxide, by inhibiting phosphorylation events of MAPK p38, Akt, phospholipase C, and protein kinase C [49]
Summary
Microglia are the resident innate immune cells in the central nervous system (CNS). Normally, microglia exist in a homeostatic “resting” state, which includes active immunosurveillance of any Antioxidants 2020, 9, 970; doi:10.3390/antiox9100970 www.mdpi.com/journal/antioxidantsAntioxidants 2020, 9, 970 danger signal. Microglia become activated upon exposure to signals from the neuronal secretome [1] or from invading pathogens [2]. Classical pro-inflammatory activation is commonly associated with neuroinflammation observed in neurodegenerative diseases [3] and is characterized by dramatic changes in canonical inflammatory-signaling cascades that induce upregulation of many cell surface receptors and cytokines, as tumor necrosis factor-alpha (TNF-α) [4]. Not disease-exclusive, these pro-inflammatory microglia are more abundant in the brains of patients suffering from neurodegenerative diseases, such as Alzheimer’s (AD) or Parkinson’s (PD) diseases [5,6]. Due to neuronal dysfunction, microglia are unable to resolve pro-inflammatory cascades and, as a consequence, excessive neuroinflammation exacerbates neurodegeneration [7]
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