Procyanidins Extracted from Lotus Seedpod Ameliorate Amyloid--Induced Toxicity in Rat Pheochromocytoma Cells.

Alzheimer's disease (AD) is a progressive neurodegenerative disease, which is characterized by extracellular senile plaque deposits, intracellular neurofibrillary tangles, and neuronal apoptosis. Amyloid- (A) plays a critical role in AD that may cause oxidative stress and downregulation of CREB/BDNF signaling. Anti-A effect has been discussed as a potential therapeutic strategy for AD. This study aimed to identify the amelioration of procyanidins extracted from lotus seedpod (LSPC) on A-induced damage with associated pathways for AD treatment. Rat pheochromocytoma (PC12) cells incubated with A serve as an A damage model to evaluate the effect of LSPC . Our findings illustrated that LSPC maintained the cellular morphology from deformation and reduced apoptosis rates of cells induced by A . The mechanisms of LSPC to protect cells from A-induced damage were based on its regulation of oxidation index and activation of CREB/BDNF signaling, including brain-derived neurotrophic factor (BDNF) and phosphorylation of cAMP-responsive element-binding (CREB), protein kinase B (also known as AKT), and the extracellular signal-regulated kinase (ERK). Of note, by high-performance liquid chromatography-tandem mass spectroscopy (LC-MS/MS), several metabolites were detected to accumulate , part of which could take primary responsibility for the amelioration of A-induced damage on PC12 cells. Taken together, our research elucidated the effect of LSPC on neuroprotection through anti-A, indicating it as a potential pretreatment for Alzheimer's disease.