Resveratrol has been reported to exert a variety of important pharmacological effects including anti-inflammatory, cardioprotective and cancer chemopreventive properties; however, its mechanisms of action are not completely understood. β-amyloid protein is considered to be responsible for the formation of senile plaques that accumulate in the brains of patients with Alzheimer disease. In the present study, we investigated the protective effect of resveratrol on β-amyloid-induced cytoxicity in cultured rat astroglioma C6 cells. Preincubation of C6 cells with resveratrol concentration-dependently protected the cells from the growth inhibition induced by β-amyloid treatment. β-amyloid treatment led to increased nitric oxide (NO) synthesis and inducible nitric oxide synthase (iNOS) expression; however, cells pretreated with resveratrol showed a dose-dependent inhibition of NO production and iNOS expression following β-amyloid treatment. Resveratrol also attenuated β-amyloid-induced prostaglandin E2 (PGE2) release, which was associated with the inhibition of cyclooxygenase (COX)-2 expression. Furthermore, β-amyloid treatment induced nuclear translocation of NF-κB, which was suppressed by resveratrol pretreatment. Collectively, the present results indicate that modulation of nuclear factor-κB (NF-κB) activity is involved in the neuroprotective action of resveratrol against β-amyloid-induced toxicity.

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