Session Title: Neurodevelopment and Neurodegeneration
MELATONIN ATTENUATES INDUCTION OF BAX- AND CASPASE-DEPENDENT DEATH SIGNALING IN METHAMPHETAMINE-TREATED HUMAN NEUROBLASTOMA SH-SY5Y CULTURED CELLS
B. Chetsawang1, W. Wisessmith1, P. Govitrapong2
Several studies demonstrate that methamphetamine-treated human neuroblastoma cells increase oxidative stress, which regulates intracellular signaling cascades leading to cell death. Melatonin has a potential as direct free radical scavenging, and protects cell death caused by methamphetamine. The objective of this study was to investigate the neuroprotective properties of melatonin on methamphetamine-induced induction of Bax- and caspase-dependent death signaling and neuronal cell degeneration in human neuroblastoma SH-SY5Y cultured cells. The results of the present study demonstrated that methamphetamine significantly decreased cell viability in SH-SY5Y cultured cells. Desipramine, a monoamine uptake blocker and melatonin was able to reverse the toxic effect of methamphetamine on reduction in cell viability. Induction of Bax, Bcl-2 and active caspase-3 protein levels were observed in SH-SY5Y cultured cells treated with methamphetamine, whereas the induction of Bax and active caspase-3 was diminished by melatonin. These finding might demonstrate important roles of Bax- and caspase-dependent death signaling and protective effects of melatonin in methamphetamine-treated neuroblastoma cells.