Heat-shock protein HSP70 protects neuroblastoma cells SK-N-SH from the neurotoxic effects of hydrogen peroxide and the β-amyloid peptide

Neuronal cell death in Alzheimer's disease is associated with the development of oxidative stress caused by the reactive oxygen species (ROS), which can be generated as a result of the effect of beta-amyloid peptides. One of the sources of ROS is hydrogen peroxide, inducing the apoptosis and necrosis of neural tissue cells. The mechanism of hydrogen peroxide apoptotic action includes launching signaling pathways that involve protein kinases PI3K, p38MAPK, JNK and ERK. Oxidative stress leads to increased synthesis of heat-shock proteins in the cells including HSP70. It was shown that the exogenous HSP70 could reduce generation of ROS in cells. In this study, we determined how HSP70 affected apoptosis and necrosis in human neuroblastoma cells SK-N-SH, induced by hydrogen peroxide and beta-amyloid peptide A beta(1-42). It was shown that HSP70 reduced the cytotoxic effects of hydrogen peroxide and beta-amyloid, and protein kinases PI3K and JNK played an important role in the mechanism of HSP70 protective effect on the peroxide induced apoptosis in SK-N-SH cells.