Poster Presentations

Session Title: Neurodevelopment and Neurodegeneration
Presentation Date: Friday, March 14 – Saturday, March 15, 2009

MELATONIN ATTENUATES INDUCTION OF BAX- AND CASPASE-DEPENDENT DEATH SIGNALING IN METHAMPHETAMINE-TREATED HUMAN NEUROBLASTOMA SH-SY5Y CULTURED CELLS

B. Chetsawang¹, W. Wisessmith¹, P. Govitrapong^2
1Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakhonpathom, Thailand, ²Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Salaya Nakhonpathom and Center for Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Bangkok, Thailand

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.