Neuroprotective effects of cyanidin against Aβ-induced oxidative and ER stress in SK-N-SH cells

This study evaluated the mechanisms underlying the protective effect of cyanidin against A beta(25-35)-induced neuronal cell death in SK-N-SH cells. A beta(25-35)-induced neurotoxicity is characterized by a decrease in cell viability, inducing the expression of endoplasmic reticulum (ER) stress proteins; an increase in intracellular reactive oxygen species (ROS) production; and an increase in intracellular calcium release. A beta(25-35) also induces neuronal toxicity through the disturbance of ER calcium levels. Pretreatment with cyanidin significantly attenuated the A beta(25-35)-induced loss of cell viability, reducing the expression of endoplasmic reticulum (ER) stress response proteins with regard to the down-regulation of the expression levels of 78 kDa glucose regulated protein (Grp78), phosphorylated forms of pancreatic ER eIF2 alpha kinase (PERK), eukaryotic initiation factor 2 alpha (eIF2 alpha), and inositol-requiring enzyme 1 (IRE1), and the expression levels of X-box binding protein 1 (XBP-1), activating transcription factor 6 (ATF6), and CCAAT/enhancer binding protein homologous transcription factor (C/EBP) homologous protein (CHOP); decreased intracellular ROS production; decreased intracellular calcium release; and reduced down regulation of the protein expression levels of calpain and cleaved caspase-12. This result suggests that cyanidin may be an alternative agent in preventing neurodegenerative diseases. (C) 2016 Elsevier Ltd. All rights reserved.