Alzheimer's disease is neuropathologically characterized by amyloid β-protein (Aβ) deposition, resulting in neurotoxicity. Herein, we focused on the prevention of anthocyanins from amyloid-mediated neurodysfunction. The data demonstrated that combined exposure of Aβ1-40 and Aβ25-35 to Neuro-2A cells resulted in reactive oxygen species (ROS) production and perturbation of calcium homeostasis. The expressions of LXRα, ApoE, ABCA1, and seladin-1 genes were significantly down-regulated upon Aβ challenge. β-Secretase, the rate-limiting enzyme that catalyzes amyloid precursor protein transform to Aβ, was up-regulated by Aβ treatment. For the duration of Aβ 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 Aβ-induced neurotoxicity through blocking ROS formation, preserving Ca2+ homeostasis, and preventing Aβ-mediated perturbation of certain genes involved in Aβ metabolism and cellular defense. The present study implicates anthocyanin as a potential therapeutic candidate for the prevention of amyloid-mediated neurodysfunction.
- Alzheimer's disease
- amyloid β-protein
- Neuro-2A cells
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)