Search

Adult neurogenesis deficiency has been proposed to be a common hallmark in different age-related neurodegenerative diseases. The administration of flavonoids is currently reported as a potentially beneficial strategy for preventing brain aging alterations, including adult neurogenesis decline. Flavonoids are a class of plant-derived dietary polyphenols that have drawn attention for their neuroprotective and pro-cognitive effects. Although they undergo extensive metabolism and localize in the brain at low concentrations, flavonoids are now believed to improve cerebral vasculature and interact with signal transduction cascades involved in the regulation of adult neurogenesis. Furthermore, many dietary flavonoids have been shown to reduce oxidative stress and neuroinflammation, improving the neuronal microenvironment where adult neurogenesis occurs. The overall goal of this review is to summarize the evidence supporting the role of flavonoids in modulating adult neurogenesis as well as to highlight how these dietary agents may be promising candidates in restoring healthy brain function during physiological and pathological aging., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Health benefits, including immune modulating capability, exerted by Bifidobacterium strains have been attributed to their exopolysaccharides (EPSs)., Objective: The effects of the purified EPS from B. longum W11 on cytokine production by peripheral blood mononuclear cells (PBMCs) alone or ConA-stimulated were investigated., Method: The production of IFN-γ, IL-1β, IL-6 and IL-10 by PBMCs from healthy adult donors was analysed using purified EPS at two different concentrations (100 µg/mL and 200 µg/mL) and ConA, as an immunopotentiating marker. Moreover, the monosaccharide composition of the EPS from B. longum W11 was detected using HPLC analysis., Results: The results demonstrated the ability of purified EPS to increase the production of the tested cytokines, except IL-10, in ConA-stimulated PBMCs. In not-stimulated-PBMCs, EPS increased the production of IL-6 (at 200 µg/mL) and IL-10 (at 100 µg/mL). The HPLC analysis showed the presence of main monomers, galactose and glucose (ratio 1:1 wt/wt), and small amount of rhamnose., Conclusion: The results of this study demonstrate the ability of the EPS produced by B. longum W11 to interact in vitro with the human PBMCs, showing an immune-regulatory profile alone and an immune stimulatory profile in ConA-stimulated PBMCs. This suggests putative applications for the EPS from B. longum W11 in different pathological conditions., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Brain aging is associated with a progressive imbalance between intracellular concentration of Reactive Oxygen Species (ROS) and cells ability to activate defensive genes. Heat Shock Protein 70 (HSP70) has been shown to act as a fundamental defensive mechanism for neurons exposed to an oxidant challenge, and its expression decreases during senescence. In the present report we show that the RNA-binding protein ELAV/HuR can affect, post-transcriptionally, the fate of HSP70 mRNA following H(2)O(2)-mediated oxidative stress in SH-SY5Y human neuroblastoma cells. As a consequence of H(2)O(2) treatment (1mM for 30 minutes), HSP70 mRNA accumulates in the ribosomes associated to the cytoskeleton, where parallel Western blotting experiments reveal statistically significant increase for both HuR and HSP70 protein levels. We also confirm the capability of HuR to bind to HSP70 mRNA, and describe how the biological effect of this ELAV protein on the HSP70 mRNA could be due to a direct phosphorylation in serine/threonine residues of HuR itself by the early (10 minutes) H(2)O(2)-mediated activation of PKC alpha. Our findings shed light on the post-transcriptional regulation of HSP70 expression, suggesting the existence of a new molecular cascade -involving PKC/HuR/HSP70- that possibly represents an early event in the cellular response to H(2)O(2)-mediated oxidative stress in SH-SY5Y human neuroblastoma cells. The present results lead us to speculate that an impairment in this regulatory mechanism might directly contribute to the defective cellular response to oxidative stress, thus helping to dissect a potential tool useful to counteract some aspects associated to cerebral senescence.