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Updated: Oct 13, 2026
Induction of Ischemic Stroke and Ischemia-reperfusion in Mice Using the Middle Artery Occlusion Technique and Visualization of Infarct Area
Published on: February 2, 2017
Pre-Ischemic Oxytocin Treatment Alleviated Neuronal Injury via Suppressing NF-κB, MMP-9, and Apoptosis Regulator
Shahein Momenabadi1,2, Abbas Ali Vafaei1,2, Mahdi Zahedi Khorasani1,2
1Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran.
Objective:
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.
Insights
Pre-ischemic administration of oxytocin (OXT) reduced stroke-induced brain injury and key inflammatory markers in mice. This suggests OXT may be a potential preventative option for cerebral stroke attacks.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Stroke is a leading cause of death and disability worldwide.
- Current treatments for stroke are limited, highlighting the need for novel therapeutic strategies.
- Oxytocin (OXT) has shown neuroprotective effects in various neurological conditions.
Purpose of the Study:
- To investigate the neuroprotective effects of pre-ischemic oxytocin (OXT) administration in a mouse model of ischemic stroke.
- To explore the molecular mechanisms underlying OXT's effects on neuronal injury, inflammation, and apoptosis.
Main Methods:
- Stroke was induced using middle cerebral artery occlusion (MCAO) in mice.
- Oxytocin (OXT) was administered intranasally for 7 days prior to MCAO.
- Infarct size, neurological deficits, spatial memory, and molecular markers (NF-κB, IL-1β, TNF-α, MMP-9, BDNF, apoptosis-related proteins) were assessed.
Main Results:
- Pre-ischemic OXT significantly reduced infarct size.
- OXT treatment decreased the expression of inflammatory markers (NF-κB, TNF-α, IL-1β, MMP-9) and apoptosis.
- OXT treatment increased the level of brain-derived neurotrophic factor (BDNF) protein.
Conclusions:
- Pre-ischemic oxytocin administration demonstrates significant neuroprotective effects in a mouse stroke model.
- OXT limits brain injury by inhibiting inflammatory pathways, MMP-9 expression, and apoptosis, while upregulating BDNF.
- Oxytocin shows potential as a preventative therapeutic agent for cerebral stroke.
