Sesaminol glucosides protect β-amyloid induced apoptotic cell death by regulating redox system in SK-N-SH cells

Abstract

We have investigated the neuroprotective effect of sesaminol glucosides (SG) in SK-N-SH cells. SG prevented apoptotic cell death induced by Aβ25-35. In parallel, SK-N-SH cells exposed to Aβ25-35 underwent oxidative stress as shown by the elevated level of intracellular ROS, lipid peroxidation, and 8-hydroxy-2′- deoxyguanosine (8-OHdG) formation, which were effectively suppressed by SG treatment. Furthermore, SG reversed the activities of catalase and glutathione peroxidase, and restored intracellular GSH levels in Aβ25-35 challenged SK-N-SH cells. In addition, SG inhibited not only Aβ25-35-induced apop- totic features including cleavage of poly(ADP-ribose) polymerase, activation of caspase-3, and activation of cas- pase-9, but also elevated Bax/Bcl-2 ratio in SK-N-SH cells treated with Aβ25-35. It was also observed that Aβ25-35 stimulated the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular protein regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAP kinase. SG inhibited phosphorylation of the JNK, ERK and p38 MAP kinase. These results suggest that SG has a protective effect against Aβ25-35-induced neuronal apoptosis, possibly through scavenging oxidative stress and regulating MAPKs signaling pathways. © Springer Science+Business Media, LLC 2011.