The present study was designed to investigate the potential neuroprotective effect of ω-conotoxin (ω-CTX) in a cell-based model of Alzheimer's disease (AD) using cultured PC12 cells incubated with β-amyloid (Aβ). Immunohistochemical staining, Western blot, MTT and TdT-mediated dUTP-biotin nick end labeling (TUNEL) analysis were employed to assess the cell viability and cell death. Aβ in this model was clearly neurotoxic, inducing necrosis and apoptosis. ω-CTX antagonized the effects of Aβ: there was an increase in cell viability and a suppression of inflammatory- and oxidative stress-related factors. These data suggest that ω-CTX may have neuroprotective actions against Aβ-induced neurotoxicity. The significance of these new findings relative to the etiology and treatment of AD is discussed.
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