Procyanidins Extracted from Lotus Seedpod Ameliorate Amyloid--Induced Toxicity in Rat Pheochromocytoma Cells.
Oxid Med Cell Longev. 2018 ;2018:4572893. Epub 2018 Oct 28. PMID: 30538801
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-Aeffect 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 Aserve as an Adamage 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.