Protective effects of silk lutein extract from Bombyx mori cocoons on β-Amyloid peptide-induced apoptosis in PC12 cells

Beta-amyloid (A beta) peptide, the hallmark of Alzheimer's disease (AD), invokes a cascade of oxidative damage to neurons and eventually leads to neuronal death. This study evaluated the protective effects of lutein extract from yellow cocoons of Bombyx mori, and its underlying mechanisms against was investigated to assess its protective effects and the underlying mechanisms against A beta(25-35)-induced neuronal cell death in cultured rat pheochromocytoma (PC12) cells. A beta(25-35)-induced neuronal toxicity is characterized by decrease in cell viability, increase in intracellular reactive oxygen species (ROS) production, activation of mitochondrial death pathway, and activation the phospholyration of mitogen-activated protein kinase (MAPKs) pathway. Pretreatment with silk lutein extract significantly attenuated A beta(25-35)-induced loss of cell viability, apoptosis, MAPKs pathway activation and ROS production. Taken together, our present study suggests that silk lutein extract protects PC12 cells from A beta(25-35)-induced neurotoxicity via the reduction of the ROS production, and subsequent attenuation of the mitochondrial death pathway and reduces the activation of the MAPK kinase pathways. This compound might beneficial as potential therapeutic agent to prevent or retard the development and progression of AD.