Effect of Oxytocin on Neuroblastoma Cell Viability and Growth

Abstract

Oxytocin, released in response to different physiological stimuli, could play a key role in reducing stress reaction. It was suggested that it has protective effect against inflammation and consequences of oxidative stress. Mechanisms how oxytocin effects mediated in the brain tissue are unclear. In this study, oxytocin effect on cell growth and neuronal viability was examined. Human neuroblastoma (SH-SY5Y and SK-N-SH) and glioblastoma (U87MG) cells were exposed to different concentrations of oxytocin for 12-96 h. Potential protective effect of oxytocin treatment was investigated after exposing cells to oxidative stress using hydrogen peroxide (50 mM, 2 h) or 6-hydroxydopamine (25 μM, 24 h). Cell proliferation was measured by cell counting and cell viability was examined by MTT assay. Protein expression of selected neurotrophic factors was measured as an additional parameter. Oxytocin (1 μM) significantly increased cell number in all three cell types. Viability of SH-SY5Y cells was increased in the presence of oxytocin without significant effect of dose (0.01-1 μM). Cell death induced by hydrogen peroxide was not prevented by incubation with oxytocin. Oxytocin pretreatment blunted neurotoxin 6-OHDA reduction of cell viability in SH-SY5Y cells. Oxytocin (1 μM, 12 h) elevated amount of total proteins without increasing levels of brain-derived neurotrophic factor and neurotrophic growth factor. In conclusion, oxytocin increases growth and viability of neuroblastoma and glioblastoma cells without activation of neurotrophic factors. Oxytocin does not have protective effect in oxidative stress; however, it might be important for neuroprotection to dopaminergic neurons. Its proliferative effect might be important in native cell life, euplastic processes, and tumor progression.

The Role of Neurotransmitters in Protection against Amyloid-β Toxicity by KiSS-1 Overexpression in SH-SY5Y Neurons

“…The SH-SY5Y neurons express oxytocin receptors [32] and oxytocin has neuroprotective actions in this cell line [33]. The effects of atosiban, an antagonist of oxytocin [34], on KiSS-1 overexpression neuroprotection against A β were therefore tested at a dose (1  μ M) that is known to be effective in cell culture models.…”

Is Oxytocin Proper for Cancer Adjuvant Therapy?

“…In conclusion, oxytocin shows slight neuroprotective effect by increasing the antioxidant capacity and stabilized oxidant status in comparison with NB cells. Bakos J and colleagues' [4] studies show 0.01-1 μM oxytocin increases neuroblastoma viability against hydrogen peroxide toxicity. Although they showed an icrease in viability, they did not report increases in neurotrophic factor levels.…”

“…OT receptors are present in the central nervous system and participates in both basic physiology and cancer pathophysiology. It was shown in brain membranes that OT has antioxidant properties, scavenging free peroxyl radicals, inhibiting LDL oxidation and lipid peroxidation [4]. Current study was designed to investigate the possible protective effect of OT against VCR and CP-induced neurotoxicity.…”

Suppression of exaggerated neuronal oscillations by oxytocin in a rat model of Parkinson’s disease

“…Indeed, many studies, both in vitro and in vivo, have suggested the cytoprotective and trophic potential of oxytocin using various experimental models (Iseri et al 2005;Ceanga et al 2010;Alizadeh et al 2012;Bakos et al 2012;Erbas et al 2012b;Leuner et al 2012). For instance, preincubation of cells with OT reduces toxicity and induce cell viability in neuronal cell cultures exposed to 6-OHDA (Bakos et al 2012). Recently, we have demonstrated the beneficial effect of OT against sepsis-induced polyneuropathy by evaluating electromyography (EMG) changes and biochemical parameters including plasma TNF-α, malondialdehyde and total anti-oxidant capacity in critical illness (Erbas et al 2013).…”

“…Besides, it elicits anti-inflammatory and anti-oxidant effects in ischemia-reperfusion injury and sepsis-induced multiple organ damage via maintaining a balance of antiinflammatory and pro-inflammatory cytokines (Iseri et al 2005;Alizadeh et al 2012). Recently, in vitro and in vivo studies have suggested the stimulatory effect of OT on cell viability against neuronal cell death (Bakos et al 2012;Leuner et al 2012).…”