Neuroprotective effect of purple rice extract and its constituent against amyloid beta-induced neuronal cell death in SK-N-SH cells

This study evaluated the protective effects of purple rice (Oryza sativa L.) extract (PRE) and its major constituent, cyanidin, and their underlying mechanisms against A beta(25-35)-induced neuronal cell death in SK-N-SH cells. A beta(25-35)-induced neuronal toxicity is characterized by decrease in cell viability, the release of lactate dehydrogenase (LDH), decrease superoxide dismutase (SOD) activity, increase in reactive oxygen species (ROS) production, morphological alteration, and activation of mitochondrial death pathway. Pretreatment with PRE and cyanidin significantly attenuated A beta(25-35)-induced loss of cell viability, apoptosis, and increase in ROS and RNS production in a dose-dependent manner. In addition, PRE and cyanidin also helped to bring about the downregulation of the expression of Bax, cytochrome c, cleavage caspase-9, and cleavage caspase-3 proteins, and the upregulation of the Bcl-X-L protein in cascade. Therefore, it is evident that PRE and its major constituent, cyanidin, were successful in protecting from the cytotoxic effect of A beta(25-35) through attenuation ROS and RNS production and modulation of mitochondrial death pathway in SK-N-SH cells. This result suggests that PRE and its major constituent, cyanidin, might be beneficial as potential therapeutic agents in preventing neurodegenerative diseases. (C) 2014 Elsevier Inc. All rights reserved.