N-Feruloyl Serotonin Attenuates Neuronal Oxidative Stress and Apoptosis in A beta(25-35)-Treated Human Neuroblastoma SH-SY5Y Cells

Amyloid-beta (A beta) aggregation and deposition have been identified as a critical feature in the pathology of Alzheimer's disease (AD), with a series of functional alterations including neuronal oxidative stress and apoptosis. N-feruloyl serotonin (FS) is a plant-derived component that exerts antioxidant activity. This study investigated the protective effects of FS on A beta(25-35)-treated neuronal damage by regulation of oxidative stress and apoptosis in human neuroblastoma SH-SY5Y cells. The radical scavenging activities increased with the concentration of FS, exhibiting in vitro antioxidant activity. The A beta(25-35)-treated SH-SY5Y cells exerted neuronal cell injury by decreased cell viability and elevated reactive oxygen species, but that was recovered by FS treatment. In addition, treatment of FS increased anti-apoptotic factor B-cell lymphoma protein 2 (Bcl-2) and decreased the pro-apoptotic factor Bcl-2-associated X protein. The FS attenuated A beta-stimulated neuronal apoptosis by regulations of mitogen-activated protein kinase signaling pathways. Moreover, activated CREB-BDNF signaling was observed by the treatment of FS in A beta(25-35)-induced SH-SY5Y cells. These results demonstrate that FS shows potential neuroprotective effects on A beta(25-35)-induced neuronal damage by attenuation of oxidative stress and apoptosis, and suggest that FS may be considered a promising candidate for the treatment of AD.