Resveratrol Protects beta Amyloid-Induced Oxidative Damage and Memory Associated Proteins in H19-7 Hippocampal Neuronal Cells

Resveratrol (trans-3, 5, 4'-trihydroxystilbene) is a polyphenolic phytoalexin known to exhibit antioxidant and neuroprotective effects in several experimental models. Amyloid beta peptide (A beta), a core component of extracellular senile plaques accumulates in the brains of patients with Alzheimer's disease and is related to the development of cognitive impairment and neuronal loss. The present study evaluates the neuroprotective action of resveratrol on A beta-induced oxidative stress and memory loss. Cultured rat hippocampal H19-7 neuronal cell line was pretreated with 75 mu M of resveratrol for 2 hrs followed by 25 mu M of A beta (1-40) for 24 hrs. H19-7 cells treated with A beta exhibited increased lipid peroxide levels. Enzymatic antioxidants including superoxide dismutase, catalase, glutathione reductase, and non-enzymatic antioxidants such as tocopherol, ascorbic acid and glutathione were decreased in the A beta treated group when compared to the control group. A beta treatment also increased the expression of total tau as well as phosphorylated forms of tau (CP13, S202/205; PHF1, S396/404) and decreased the expression of insulin degrading enzyme (IDE), phosphoglycogen synthase kinase 3 beta involved in A beta degradation and tau hyper phosphorylation. Expression of PSD-95 and Arc proteins, essential for synaptic maturity and plasticity, was decreased by A beta treatment. Resveratrol treatment attenuated the accumulation of lipid peroxide levels, up-regulated the antioxidant activities and improved the expression of memory-associated proteins in A beta treated H19-7 cells. These findings highlight the neuroprotective effect of resveratrol in preventing A beta-induced oxidative damage and memory loss in vitro.