Resveratrol protects against experimental stroke: Putative neuroprotective role of heme oxygenase 1
and the negative part here:
http://www.jbc.org/content/early/2012/10/26/jbc.M112.406413.short
Abstract
Resveratrol is a phytoalexin and natural
phenol that is present at relatively high concentrations in peanuts and
red grapes
and wine. Based upon studies of yeast and
invertebrate models, it has been proposed that ingestion of resveratrol
may have
anti-aging actions in mammals including humans. It
has also been suggested that resveratrol exerts its beneficial effects
on health by activating the same cellular signaling
pathways that are activated by dietary energy restriction (DR). Some
studies
have reported therapeutic actions of resveratrol in
animal models of metabolic neurodegenerative disorders. However, the
effects
of resveratrol on cell, tissue and organ function
in healthy subjects are largely unknown. In the present study, we
evaluated
the potential effects of resveratrol on the
proliferation and survival of neural progenitor cells (NPCs) in culture,
and in
the hippocampus of healthy young adult mice.
Resveratrol reduced the proliferation of cultured mouse multi-potent
NPCs, and
activated AMP-activated protein kinase (AMPK), in a
concentration-dependent manner. Administration of resveratrol to mice
(1-10 mg/kg) resulted in activation of AMPK, and
reduced the proliferation and survival of NPCs in the dentate gyrus of
the
hippocampus. Resveratrol down-regulated the levels
of the phosphorylated form of cyclic AMP response element-binding
protein
(pCREB) and brain-derived neurotrophic factor
(BDNF) in the hippocampus. Finally, resveratrol-treated mice exhibited
deficits
in hippocampus-dependent spatial learning and
memory. Our findings suggest that resveratrol, unlike DR, adversely
affects
hippocampal neurogenesis and cognitive function by a
mechanism involving activation of AMPK and suppression of CREB and BDNF
signaling.
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