Anti-Apoptotic Effect of Selegiline as Monoamine Oxidase Inhibitor on Rat Hippocampus Derived Neural Stem Cells in Oxidative Stress Condition

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.
The neural stem cells were isolated from the hippocampi of neonatal rats then pretreated with different doses of selegiline for 48 hours while later being exposed to 125μM H2O2 for 30 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.
The results showed that apoptosis rate was significantly decreased in 10-7 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.
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.