Neuroprotective effects of N-acetylglucosamine against hydrogen peroxide-induced apoptosis in human neuronal SK-N-SH cells by inhibiting the activation of caspase-3, PARP, and p38

Neuroprotective effects of N-acetylglucosamine (GlcNAc), a monosaccharide derivative of glucose, against H2O2-induced neurotoxicity and its underlying mechanism in human SK-N-SH neuroblastoma cells were investigated. Pretreatment of GlcNAc prior to exposure of cells to H2O2 stress significantly reduced the H2O2-mediated neuronal cell death and apoptosis. The GlcNAc dose-dependently decreased the level of intracellular reactive oxygen species (ROS) in H2O2-treated cells and also effectively inhibited H2O2-induced apoptotic features such as DNA fragmentation, caspase-3, and poly ADP-ribose polymerase (PARP) cleavages, and p38 phosphorylation. These results suggested that GlcNAc might potentially serve as agents for prevention of neurodegenerative diseases caused by oxidative stresses and this effect may be associated with the suppression of caspase-3, PARP, and p38 activation.