http://www.springerlink.com/index/r4262145087m7587.pdf
Abstract
Glutamate excitotoxicity is involved in many neurodegenerative diseases including Alzheimer’s disease (AD). Attenuation of
glutamate toxicity is one of the therapeutic strategies for AD. Wolfberry (Lycium barbarum)
is a common ingredient in oriental cuisines. A number of studies
suggest that wolfberry has anti-aging properties. In recent
years, there is a trend of using dried Wolfberry as food
supplement and health product in UK and North America. Previously,
we have demonstrated that a fraction of polysaccharide from
Wolfberry (LBA) provided remarkable neuroprotective effects against
beta-amyloid peptide-induced cytotoxicity in primary cultures
of rat cortical neurons. To investigate whether LBA can protect
neurons from other pathological factors such as glutamate found
in Alzheimer brain, we examined whether it can prevent neurotoxicity
elicited by glutamate in primary cultured neurons. The
glutamate-induced cell death as detected by lactate dehydrogenase assay
and caspase-3-like activity assay was significantly reduced by
LBA at concentrations ranging from 10 to 500 μg/ml. Protective
effects of LBA were comparable to memantine, a non-competitive
NMDA receptor antagonist. LBA provided neuroprotection even
1 h after exposure to glutamate. In addition to glutamate, LBA
attenuated N-methyl-d-aspartate (NMDA)-induced neuronal damage. To further explore whether LBA might function as antioxidant, we used hydrogen
peroxide (H2O2) as oxidative stress inducer in this study. LBA could not attenuate the toxicity of H2O2.
Furthermore, LBA did not attenuate glutamate-induced oxidation by using
NBT assay. Western blot analysis indicated that
glutamate-induced phosphorylation of c-jun N-terminal kinase
(JNK) was reduced by treatment with LBA. Taken together, LBA
exerted significant neuroprotective effects on cultured
cortical neurons exposed to glutamate.
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