Neuroglobin protects PC12 cells against β-amyloid-induced cell injury

Abstract Excessive accumulation of amyloid beta (Aβ) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. Possible mechanisms underlying Aβ-induced neuronal cytotoxicity include excess production of reactive oxidative species (ROS) and apoptosis. Neuroglobin (Ngb), a newly discovered globin in vertebrates that exhibits neuroprotective functions, may have a potential role in scavenging ROS. To examine the potential protective role of Ngb in Aβ-induced cytotoxicity, PC12 cells were treated with Aβ (1-42 fragment) for 24 h. Aβ treatments increased ROS production in PC12 cells. Overexpression of Ngb but not Ngb mutant in the PC12 cells significantly attenuated Aβ-induced ROS production and lipids peroxidation. Furthermore, overexpression of Ngb also attenuated Aβ-induced mitochondrial dysfunction and apoptosis, and promoted cell survival in PC12 cells. Therefore, Ngb may act as an intracellular ROS scavenger, and such antioxidant properties may play a protective role against Aβ-induced cell injury.