Protective Effects of Anthocyan ins against Amyloid β-Peptide-Induced Damage in Neuro-2A Cells

Alzheimer's disease is neuropathologically characterized by amyloid beta-protein (A beta) deposition, resulting in neurotoxicity. Herein, we focused on the prevention of anthocyanins from amyloid-mediated neurodysfunction. The data demonstrated that combined exposure of A beta(1-40) and A beta(25-35) to Neuro-2A cells resulted in reactive oxygen species (ROS) production and perturbation of calcium homeostasis. The expressions of LXR alpha, ApoE, ABCA1, and seladin-1 genes were significantly clown-regulated upon A beta challenge. beta-Secretase, the rate-limiting enzyme that catalyzes amyloid precursor protein transform to A beta, was up-regulated by A beta treatment. For the duration of A beta stimulation, malvidin (Mal) or oenin (Oen; malvidin-3-O-glucoside) was added, and the protective effects were observed. Mal and Oen showed protective effects against A beta-induced neurotoxicity through blocking ROS formation, preserving Ca2+ homeostasis, and preventing A beta-mediated perturbation of certain genes involved in A beta metabolism and cellular defense. The present study implicates anthocyanin as a potential therapeutic candidate for the prevention of amyloid-mediated neurodysfunction.