pre-ischemic oxytocin treatment alleviated neuronal injury via suppressing nf-κb, mmp-9, and apoptosis regulator proteins in a mice model of stroke

Objectives: this study was designed to determine the effects of pre-ischemic administration of oxytocin (oxt) on neuronal injury and possible molecular mechanisms in a mice model of stroke. materials and methods: in this experimental study, stroke was induced in the mice by middle cerebral artery occlusion (mcao) for 60 minutes and 24 hours of reperfusion. oxt was given as intranasal daily for 7 consecutive days before ischemic stroke. neuronal damage, spatial memory, and the expression levels of nuclear factor-kappa b (nf-κb), interleukin-1β (il-1β), tumor necrosis factor-α (tnf-α), matrix metalloproteinase-9 (mmp-9), brain-derived neurotrophic factor (bdnf) and apoptosis were assessed 24 hours after stroke. results: pre-ischemic treatment with oxt significantly reduced the infarct size (p<0.01); but did not recover the neurological and spatial memory dysfunction (p>0.05). moreover, oxt treatment considerably decreased the expressions of nf-κb, tnf-α, il-1β, and mmp-9 (p<0.001) and enhanced the level of bdnf protein. oxt treatment also significantly downregulated bax expression and overexpressed bcl-2 proteins. conclusion: the finding of this study indicated that administration of oxt before ischemia could limit brain injury by inhibiting mmp-9 expression, apoptosis, inflammatory signaling pathways, and an increase in the bdnf protein level. we suggested that oxt may be potentially useful in the prevention and/or reducing the risk of the cerebral stroke attack, and could be offered as a new prevention option in the clinics.