علی نیک فر - Dept. of Genetics and Molecular Medicine, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
علیرضا عبدانی پور - دانشکده پزشکی، دانشگاه علوم پزشکی زنجان، زنجان
معصومه قلی نژاد - Dept. of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

Background and Objective: Damaged and inflammatory cells in the nervous system produce reactive oxygen species (ROS). The overproduction of ROS can cause serious damage to important biomolecules and over activation of programmed cell death leads to many progressive neurodegenerative disorders. The aim of this study was to evaluate the effects of selegiline on inhibition of apoptosis in oxidative damage induced by hydrogen peroxide in rat hippocampus derived neural stem cells. Materials and Methods: The neural stem cells were isolated from the hippocampi of neonatal rats then pretreated with different doses of selegiline for ۴۸ hours while later being exposed to ۱۲۵μM H۲O۲ for ۳۰ min. Using MTT assay and TUNEL staining, we evaluated the effects of selegiline on cell survival and apoptosis in pretreated NSCs compared to control groups. Also, the induction of NSCs to neuron-like cells was evaluated using Nissl staining. Results: The results showed that apoptosis rate was significantly decreased in ۱۰-۷ M of selegiline pretreated NSCs compared to the control group. Also, the mean percentage of Nissl positive cells significantly increased in selegiline pretreated neural stem cells compared to the control group. Conclusion: Our findings suggest that selegiline protects NSCs against oxidative stress induced cell death, and therefore, it may be used to promote the survival rate of NSCs and can be a candidate for treatment of oxidative stress-mediated neurological diseases.

Neural stem cells, Selegiline, Oxidative stress, Apoptosis